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Massive GI bleeding due to a duodenal arteriovenous malformation
Massive GI bleeding due to duodenal arteriovenous malformation
Massive GI bleeding due to a duodenal arteriovenous malformation Ronnie Tung-Ping Poon, MBBS, FRCS(Edin), Jensen Poon, MBBS
Arteriovenous malformation (AVM) of the GI tract has become a frequently recognized cause of GI bleeding due to the widespread use of visceral angiography. However, duodenal AVM is rare and represents a unique challenge for diagnosis and therapy. We report a case of massive GI bleeding due to a duodenal AVM initially misdiagnosed as a duodenal varix. CASE REPORT A 47-year-old man was admitted because of melena. He was a chronic alcoholic, but otherwise his medical and family histories were unremarkable. On admission, he was pale, tachycardiac (120/min), and hypotensive (90/50 mm Hg). There was no obvious cutaneous, mucosal, or bony abnormality. Abdominal examination was normal. His hemoglobin level was 6.5 g/dL (normal 13.0-16.5), and he was resuscitated with blood transfusion. Upper endoscopy immediately after admission showed a normal esophagus and stomach and a large submucosal tortuous vessel of about 1 cm in size with active bleeding From the Department of Surgery, The University of Hong Kong Medical Centre, Queen Mary Hospital, Hong Kong, China. Reprint requests: Ronnie Tung-Ping Poon, MBBS, FRCS(Edin), Department of Surgery, Queen Mary Hospital, Pokfulam Road, Hong Kong, China. Copyright © 2000 by the American Society for Gastrointestinal Endoscopy 0016-5107/2000/$12.00 + 0 37/4/106107 doi:10.1067/mge.2000.106107 VOLUME 52, NO. 1, 2000
R Poon, J Poon
in the second part of the duodenum (Fig. 1). The lesion was thought to be a duodenal varix because of its appearance and the history of alcoholism. The lesion was injected with a mixture of Histoacryl (butyl 2-cyanoacrylate; Braun, Melsungen, Germany) (1 mL) and Lipiodol (1 mL), and the bleeding was controlled. The patient’s hemodynamic status improved and his hemoglobin level increased to 10 g/dL after 4 units of blood transfusion. Subsequently, his liver function tests, platelet count, and coagulation profile all returned to normal. Abdominal US did not reveal any evidence of cirrhosis or portal hypertension. In light of the normal liver function tests and US, an AVM was suspected and the patient was scheduled for an arteriography the next day. He remained stable overnight, but the next morning he had recurrent massive melena with a drop of blood pressure to 80/40 mm Hg. The hemoglobin level dropped to 5.5 g/dL and he was transfused with a further 4 units of blood. Arteriography revealed a large AVM at the second part of the duodenum arising from the gastroduodenal artery (Fig 2). No active bleeding could be demonstrated at arteriography, but the artery was nevertheless embolized using Gelfoam. The patient remained in shock with further melena after embolization, hence an emergency laparotomy was performed. Duodenotomy revealed a large tortuous submucosal vessel on the posteromedial aspect of the second part of the duodenum with active bleeding. Resection of the AVM would entail pancreatoduodenectomy, which was considered too hazardous, as the patient was hemodynamically unstable. The gastroduodenal artery was isolated, ligated, and divided. The submucosal vessel immediately shrank in size and bleeding was controlled easily with plication. He recovered uneventfully and was discharged 1 week later. He has remained asymptomatic, and upper endoscopy 3 years later did not reveal any evidence of recurrence of the lesion in the duodenum. GASTROINTESTINAL ENDOSCOPY
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R Poon, J Poon
Massive GI bleeding due to duodenal arteriovenous malformation
Figure 1. Endoscopic appearance of the duodenal AVM. The large submucosal tortuous vessel (arrow) was misdiagnosed as a duodenal varix. Active oozing of blood was seen at endoscopy.
DISCUSSION
Figure 2. Selective arteriography showing an AVM arising from the gastroduodenal artery (arrow), with characteristic racemose vascular network and early venous filling. Note the size of the dilated gastroduodenal artery compared with the hepatic artery.
Gastrointestinal AVMs encompass a spectrum of vascular abnormalities, ranging from a cluster of abnormal mucosal vessels to a vascular malformation involving a major artery.1 Moore et al.2 classified these lesions into three types based on patient age, location, macroscopic appearance, and family history. Type 1 lesions usually occur in elderly patients as a small solitary lesion primarily in the right colon and may not be visible grossly. These lesions are thought to be acquired and are commonly termed angiodysplasia or vascular ectasia. The exact pathogenesis is unknown but it has been postulated that they are degenerative in nature.3 They are commonly associated with chronic medical conditions such as aortic valve disease and von Willebrand’s disease.4-6 Type 2 AVMs occur in younger patients, most commonly in the small bowel and are often visible grossly as a large submucosal vessel. This type of lesion is thought to be congenital in origin. Lesions of hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber syndrome) are classified as type 3 and are associated with respiratory and cutaneous lesions. A review by Cavett et al.7 of 47 cases of GI AVMs reported before 1976 found that the most common location of AVMs was the right colon, followed by small intestine, and in only two cases were lesions located in the duodenum.7 Subsequent to this review, 28 more cases of duodenal AVMs have been reported in English language publications.5,6,8-16 However, the majority of these reported cases were type 1 lesions that are similar to angiodysplasia in the colon. They were usually described as small, bright red, and well-circumscribed mucosal lesions,
some of which were not visible at endoscopy. Our case is considered to be a type 2 AVM of congenital origin according to the classification of Moore et al. Most cases of duodenal AVMs reported presented with either chronic blood loss or recurrent bleeding. Acute massive bleeding leading to hemodynamic compromise as in our case is extremely unusual. To our knowledge, a duodenal AVM with the endoscopic appearance of a large dilated submucosal vessel as seen in our patient has not been described before. Bleeding from a large duodenal cavernous hemangioma that also appeared as a submucosal protruding lesion has been reported, but this is a pathologically distinct entity.17 Cavernous hemangioma is a benign vascular neoplasm composed histologically of large cavernous vascular channels,17 whereas AVMs are not neoplasms but rather errors in vascular morphogenesis, and they appear histologically as tangles of abnormal vessels of various sizes that have characteristics of arteries and veins. Clinical differentiation between these two rare conditions could be difficult because of similar endoscopic appearances. Angiography may help in diagnosis. An AVM is characterized by a large feeding artery, a racemose vascular network (branching with nodular terminations), and early filling in the venous phase. In contrast, a cavernous hemangioma is characterized by a normal-sized artery feeding an area of vascular lakes, with pooling of the contrast late into the venous phase. The diagnosis of a duodenal AVM of the angiodysplasia type can often be made by the characteristic endoscopic appearance. In our case, the endoscopic
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VOLUME 52, NO. 1, 2000
Massive GI bleeding due to duodenal arteriovenous malformation
R Poon, J Poon
appearance of the AVM mimicked a duodenal varix which led to an incorrect diagnosis initially. The successful control of bleeding with Histoacryl injection resulted in a false sense of security, and there was some delay in obtaining an angiography. Duodenal AVM and varix are both extremely rare causes of upper GI bleeding, but their differentiation is of great importance because of differences in the approach to management. Our case serves to emphasize the importance of early angiography in upper GI bleeding from lesions of uncertain nature. The angiographic appearance is diagnostic of AVM. Endoscopic Doppler US has been found useful in the diagnosis of GI AVMs,18 but angiography remains the reference standard and it provides a vascular map that is essential for planning management. Therapeutic endoscopy with injection of hemostatic agents, heat probe coagulation or laser photocoagulation is the first-line treatment for a small mucosal vascular lesion and any of these methods can usually control the bleeding.1,4,8,9 However, these forms of treatment are less likely to be successful for a large submucosal vessel as in the present case. Histoacryl injection has been used successfully to achieve hemostasis in duodenal variceal bleeding and other causes of upper GI bleeding.19,20 Its use in a bleeding duodenal AVM has not been documented before, but in our patient its hemostatic effect was only transient. It could possibly be used as a temporizing endoscopic measure for control of bleeding, but more definitive therapy should follow. Successful angiographic management of duodenal AVM by embolization has been reported and it can be used as a definitive treatment, especially in highrisk patients.11,12 In our patient, embolization using Gelfoam did not control the hemorrhage. This may be related in part to the large size of the lesion. A steel coil is an alternative material for embolization and may produce more complete occlusion, but recurrent bleeding is still possible.12 Vasoconstricting agents such as vasopressin have been used to supplement embolization.12 Surgical excision has been the mainstay of treatment in the majority of reported cases of GI AVMs described in the literature.2,7,10,13,15 Where possible, AVMs should be excised to prevent recurrence. Excision of small mucosal AVMs in the first part of the duodenum has been reported.10,13 Surgical excision is also considered the treatment of choice for GI cavernous hemangioma, and successful treatment of a bleeding hemangioma in the fourth part of the duodenum by wedge excision has been described.17 In our patient, with a large submucosal lesion in the posteromedial wall of the second part of the duodenum, surgical resection would have entailed pancre-
atoduodenectomy. Because of the patient’s unstable hemodynamic status, this would have been a major procedure with substantial risk. Ligation of the feeding gastroduodenal artery proved to be an effective life-saving option. There has been no previous report of this surgical approach for a large duodenal AVM as in our case, and the long-term result is still unknown. Recurrence of the AVM by development of collateral arteries is a concern, but in our patient there has been no evidence of recurrence after 3 years. In the case of future recurrence, a resection by pancreatoduodenectomy may be indicated. Pancreatoduodenectomy for the treatment of AVMs arising in the head of the pancreas with involvement of the duodenum has been described in stable patients presenting with more chronic or recurrent bleeding.21,22
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REFERENCES 1. Katz PO, Salas L. Less frequent causes of upper gastrointestinal bleeding. Gastroenterol Clin North Am 1993;22:875-89. 2. Moore JD, Thompson NW, Appelman HD, Foley D. Arteriovenous malformations of gastrointestinal tract. Arch Surg 1976;111:381-9. 3. Boley SJ, Sammartano RJ, Adams A, DiBiase A, Kleinhaus S, Sprayregen S. On the nature and etiology of vascular ectasias of the colon. Degenerative lesions of aging. Gastroenterology 1977;72:650-60. 4. Rogers BHG. Endoscopic diagnosis and therapy of mucosal vascular abnormalities of the gastrointestinal tract occurring in elderly patients and associated with cardiac, vascular and pulmonary disease. Gastrointest Endosc 1980;26:134-8. 5. Weaver GA, Alpern HD, Davis JS, Ramsey WH, Peichelderfer H. Gastrointestinal angiodysplasia associated with aortic valve disease. Part of the spectrum of angiodysplasia of the gut. Gastroenterology 1979;77:1-11. 6. Duray PH, Marcal JM Jr, LiVolsi VA, Fisher R, Scholhamer C, Brand MH. Gastrointestinal angiodysplasia: a possible component of von Willebrand’s disease. Hum Pathol 1984;15:539-44. 7. Cavett CM, Selby JH, Hamilton JL, Williamson JW. Arteriovenous malformation in chronic gastrointestinal bleeding. Ann Surg 1977;185:116-21. 8. Gunnlaugsson O. Angiodysplasia of the stomach and duodenum. Gastrointest Endosc 1985;31:251-4. 9. Marwick T, Kerlin P. Angiodysplasia of the upper gastrointestinal tract. Clinical spectrum in 41 cases. J Clin Gastroenterol 1986;8:404-7. 10. Lewis JW, Mason EE, Jochimsen PR. Vascular malformations of the stomach and duodenum. Surg Gynecol Obstet 1981; 153:225-8. 11. Goldin AR, Dent DM, Davies PG. Angiography in the diagnosis and management of duodenal arteriovenous malformation. A case report. S Afr Med J 1979;55:347-8. 12. Granmayeh M, Wallace S, Schwarten D. Transcatheter occlusion of the gastroduodenal artery. Radiology 1979;131:59-64. 13. Stallwood GR, Richards TA. Arteriovenous malformation of the duodenum. Can J Surg 1980;23:572-4. 14. Goff WB, Rosenkrantz H, Healy JF. Angiographic demonstration of bleeding duodenal arteriovenous malformation. J Am Osteopath Assoc 1982;82:189-91. 15. Fowler DL, Fortin D, Wood WG, Pinkerton JA Jr, Koontz PG Jr. Intestinal vascular malformations. Surgery 1979;86:377-85. GASTROINTESTINAL ENDOSCOPY
103
16. Criando KJ, Shureigh SF, Howard WH, Wilson TH Jr. Arteriovenous malformations of the duodenum: a report of three cases. Md State Med J 1982;31:63-5. 17. Fujikawa T, Kurata M, Takaori K, Matsusue S, Takeda H, Sakai S. Solitary cavernous hemangioma of the duodenum: report of a case. Surg Today 1996;26:807-9. 18. Rutgeerts P, Vantrappen G, D’Heygere F, Broeckaert L. Transendoscopic Doppler ultrasound: usefulness for diagnosis and treatment of vascular malformations. Endoscopy 1988;20:99-101. 19. Labenz J, Borsch G. Successful endoscopic haemostasis of duodenal variceal bleeding with Histoacryl [letter]. Endoscopy 1993;25:194.
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20. Kok KYY, Kum CK, Goh PMY. Endoscopic hemostasis of upper gastrointestinal bleeding with histoacryl: last resort before surgery. Endoscopy 1996;28:256-8. 21. Takiguchi N, Ichiki N, Ishige H, Yamazaki T, Sarashina H, Suzuki I, et al. Pancreatic arteriovenous malformation involving adjacent duodenum in a patient with gastrointestinal bleeding. Am J Gastroenterol 1995;90:1151-4. 22. Shahrudin MD, Noori SM. Management of a rare case of arteriovenous malformation of the head of the pancreas. Hepatogastroenterology 1997;44:284-7.
VOLUME 52, NO. 1, 2000
Massive GI bleeding due to a duodenal arteriovenous malformation Ronnie Tung-Ping Poon, MBBS, FRCS(Edin), Jensen Poon, MBBS
Arteriovenous malformation (AVM) of the GI tract has become a frequently recognized cause of GI bleeding due to the widespread use of visceral angiography. However, duodenal AVM is rare and represents a unique challenge for diagnosis and therapy. We report a case of massive GI bleeding due to a duodenal AVM initially misdiagnosed as a duodenal varix. CASE REPORT A 47-year-old man was admitted because of melena. He was a chronic alcoholic, but otherwise his medical and family histories were unremarkable. On admission, he was pale, tachycardiac (120/min), and hypotensive (90/50 mm Hg). There was no obvious cutaneous, mucosal, or bony abnormality. Abdominal examination was normal. His hemoglobin level was 6.5 g/dL (normal 13.0-16.5), and he was resuscitated with blood transfusion. Upper endoscopy immediately after admission showed a normal esophagus and stomach and a large submucosal tortuous vessel of about 1 cm in size with active bleeding From the Department of Surgery, The University of Hong Kong Medical Centre, Queen Mary Hospital, Hong Kong, China. Reprint requests: Ronnie Tung-Ping Poon, MBBS, FRCS(Edin), Department of Surgery, Queen Mary Hospital, Pokfulam Road, Hong Kong, China. Copyright © 2000 by the American Society for Gastrointestinal Endoscopy 0016-5107/2000/$12.00 + 0 37/4/106107 doi:10.1067/mge.2000.106107 VOLUME 52, NO. 1, 2000
R Poon, J Poon
in the second part of the duodenum (Fig. 1). The lesion was thought to be a duodenal varix because of its appearance and the history of alcoholism. The lesion was injected with a mixture of Histoacryl (butyl 2-cyanoacrylate; Braun, Melsungen, Germany) (1 mL) and Lipiodol (1 mL), and the bleeding was controlled. The patient’s hemodynamic status improved and his hemoglobin level increased to 10 g/dL after 4 units of blood transfusion. Subsequently, his liver function tests, platelet count, and coagulation profile all returned to normal. Abdominal US did not reveal any evidence of cirrhosis or portal hypertension. In light of the normal liver function tests and US, an AVM was suspected and the patient was scheduled for an arteriography the next day. He remained stable overnight, but the next morning he had recurrent massive melena with a drop of blood pressure to 80/40 mm Hg. The hemoglobin level dropped to 5.5 g/dL and he was transfused with a further 4 units of blood. Arteriography revealed a large AVM at the second part of the duodenum arising from the gastroduodenal artery (Fig 2). No active bleeding could be demonstrated at arteriography, but the artery was nevertheless embolized using Gelfoam. The patient remained in shock with further melena after embolization, hence an emergency laparotomy was performed. Duodenotomy revealed a large tortuous submucosal vessel on the posteromedial aspect of the second part of the duodenum with active bleeding. Resection of the AVM would entail pancreatoduodenectomy, which was considered too hazardous, as the patient was hemodynamically unstable. The gastroduodenal artery was isolated, ligated, and divided. The submucosal vessel immediately shrank in size and bleeding was controlled easily with plication. He recovered uneventfully and was discharged 1 week later. He has remained asymptomatic, and upper endoscopy 3 years later did not reveal any evidence of recurrence of the lesion in the duodenum. GASTROINTESTINAL ENDOSCOPY
101
R Poon, J Poon
Massive GI bleeding due to duodenal arteriovenous malformation
Figure 1. Endoscopic appearance of the duodenal AVM. The large submucosal tortuous vessel (arrow) was misdiagnosed as a duodenal varix. Active oozing of blood was seen at endoscopy.
DISCUSSION
Figure 2. Selective arteriography showing an AVM arising from the gastroduodenal artery (arrow), with characteristic racemose vascular network and early venous filling. Note the size of the dilated gastroduodenal artery compared with the hepatic artery.
Gastrointestinal AVMs encompass a spectrum of vascular abnormalities, ranging from a cluster of abnormal mucosal vessels to a vascular malformation involving a major artery.1 Moore et al.2 classified these lesions into three types based on patient age, location, macroscopic appearance, and family history. Type 1 lesions usually occur in elderly patients as a small solitary lesion primarily in the right colon and may not be visible grossly. These lesions are thought to be acquired and are commonly termed angiodysplasia or vascular ectasia. The exact pathogenesis is unknown but it has been postulated that they are degenerative in nature.3 They are commonly associated with chronic medical conditions such as aortic valve disease and von Willebrand’s disease.4-6 Type 2 AVMs occur in younger patients, most commonly in the small bowel and are often visible grossly as a large submucosal vessel. This type of lesion is thought to be congenital in origin. Lesions of hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber syndrome) are classified as type 3 and are associated with respiratory and cutaneous lesions. A review by Cavett et al.7 of 47 cases of GI AVMs reported before 1976 found that the most common location of AVMs was the right colon, followed by small intestine, and in only two cases were lesions located in the duodenum.7 Subsequent to this review, 28 more cases of duodenal AVMs have been reported in English language publications.5,6,8-16 However, the majority of these reported cases were type 1 lesions that are similar to angiodysplasia in the colon. They were usually described as small, bright red, and well-circumscribed mucosal lesions,
some of which were not visible at endoscopy. Our case is considered to be a type 2 AVM of congenital origin according to the classification of Moore et al. Most cases of duodenal AVMs reported presented with either chronic blood loss or recurrent bleeding. Acute massive bleeding leading to hemodynamic compromise as in our case is extremely unusual. To our knowledge, a duodenal AVM with the endoscopic appearance of a large dilated submucosal vessel as seen in our patient has not been described before. Bleeding from a large duodenal cavernous hemangioma that also appeared as a submucosal protruding lesion has been reported, but this is a pathologically distinct entity.17 Cavernous hemangioma is a benign vascular neoplasm composed histologically of large cavernous vascular channels,17 whereas AVMs are not neoplasms but rather errors in vascular morphogenesis, and they appear histologically as tangles of abnormal vessels of various sizes that have characteristics of arteries and veins. Clinical differentiation between these two rare conditions could be difficult because of similar endoscopic appearances. Angiography may help in diagnosis. An AVM is characterized by a large feeding artery, a racemose vascular network (branching with nodular terminations), and early filling in the venous phase. In contrast, a cavernous hemangioma is characterized by a normal-sized artery feeding an area of vascular lakes, with pooling of the contrast late into the venous phase. The diagnosis of a duodenal AVM of the angiodysplasia type can often be made by the characteristic endoscopic appearance. In our case, the endoscopic
102
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VOLUME 52, NO. 1, 2000
Massive GI bleeding due to duodenal arteriovenous malformation
R Poon, J Poon
appearance of the AVM mimicked a duodenal varix which led to an incorrect diagnosis initially. The successful control of bleeding with Histoacryl injection resulted in a false sense of security, and there was some delay in obtaining an angiography. Duodenal AVM and varix are both extremely rare causes of upper GI bleeding, but their differentiation is of great importance because of differences in the approach to management. Our case serves to emphasize the importance of early angiography in upper GI bleeding from lesions of uncertain nature. The angiographic appearance is diagnostic of AVM. Endoscopic Doppler US has been found useful in the diagnosis of GI AVMs,18 but angiography remains the reference standard and it provides a vascular map that is essential for planning management. Therapeutic endoscopy with injection of hemostatic agents, heat probe coagulation or laser photocoagulation is the first-line treatment for a small mucosal vascular lesion and any of these methods can usually control the bleeding.1,4,8,9 However, these forms of treatment are less likely to be successful for a large submucosal vessel as in the present case. Histoacryl injection has been used successfully to achieve hemostasis in duodenal variceal bleeding and other causes of upper GI bleeding.19,20 Its use in a bleeding duodenal AVM has not been documented before, but in our patient its hemostatic effect was only transient. It could possibly be used as a temporizing endoscopic measure for control of bleeding, but more definitive therapy should follow. Successful angiographic management of duodenal AVM by embolization has been reported and it can be used as a definitive treatment, especially in highrisk patients.11,12 In our patient, embolization using Gelfoam did not control the hemorrhage. This may be related in part to the large size of the lesion. A steel coil is an alternative material for embolization and may produce more complete occlusion, but recurrent bleeding is still possible.12 Vasoconstricting agents such as vasopressin have been used to supplement embolization.12 Surgical excision has been the mainstay of treatment in the majority of reported cases of GI AVMs described in the literature.2,7,10,13,15 Where possible, AVMs should be excised to prevent recurrence. Excision of small mucosal AVMs in the first part of the duodenum has been reported.10,13 Surgical excision is also considered the treatment of choice for GI cavernous hemangioma, and successful treatment of a bleeding hemangioma in the fourth part of the duodenum by wedge excision has been described.17 In our patient, with a large submucosal lesion in the posteromedial wall of the second part of the duodenum, surgical resection would have entailed pancre-
atoduodenectomy. Because of the patient’s unstable hemodynamic status, this would have been a major procedure with substantial risk. Ligation of the feeding gastroduodenal artery proved to be an effective life-saving option. There has been no previous report of this surgical approach for a large duodenal AVM as in our case, and the long-term result is still unknown. Recurrence of the AVM by development of collateral arteries is a concern, but in our patient there has been no evidence of recurrence after 3 years. In the case of future recurrence, a resection by pancreatoduodenectomy may be indicated. Pancreatoduodenectomy for the treatment of AVMs arising in the head of the pancreas with involvement of the duodenum has been described in stable patients presenting with more chronic or recurrent bleeding.21,22
VOLUME 52, NO. 1, 2000
REFERENCES 1. Katz PO, Salas L. Less frequent causes of upper gastrointestinal bleeding. Gastroenterol Clin North Am 1993;22:875-89. 2. Moore JD, Thompson NW, Appelman HD, Foley D. Arteriovenous malformations of gastrointestinal tract. Arch Surg 1976;111:381-9. 3. Boley SJ, Sammartano RJ, Adams A, DiBiase A, Kleinhaus S, Sprayregen S. On the nature and etiology of vascular ectasias of the colon. Degenerative lesions of aging. Gastroenterology 1977;72:650-60. 4. Rogers BHG. Endoscopic diagnosis and therapy of mucosal vascular abnormalities of the gastrointestinal tract occurring in elderly patients and associated with cardiac, vascular and pulmonary disease. Gastrointest Endosc 1980;26:134-8. 5. Weaver GA, Alpern HD, Davis JS, Ramsey WH, Peichelderfer H. Gastrointestinal angiodysplasia associated with aortic valve disease. Part of the spectrum of angiodysplasia of the gut. Gastroenterology 1979;77:1-11. 6. Duray PH, Marcal JM Jr, LiVolsi VA, Fisher R, Scholhamer C, Brand MH. Gastrointestinal angiodysplasia: a possible component of von Willebrand’s disease. Hum Pathol 1984;15:539-44. 7. Cavett CM, Selby JH, Hamilton JL, Williamson JW. Arteriovenous malformation in chronic gastrointestinal bleeding. Ann Surg 1977;185:116-21. 8. Gunnlaugsson O. Angiodysplasia of the stomach and duodenum. Gastrointest Endosc 1985;31:251-4. 9. Marwick T, Kerlin P. Angiodysplasia of the upper gastrointestinal tract. Clinical spectrum in 41 cases. J Clin Gastroenterol 1986;8:404-7. 10. Lewis JW, Mason EE, Jochimsen PR. Vascular malformations of the stomach and duodenum. Surg Gynecol Obstet 1981; 153:225-8. 11. Goldin AR, Dent DM, Davies PG. Angiography in the diagnosis and management of duodenal arteriovenous malformation. A case report. S Afr Med J 1979;55:347-8. 12. Granmayeh M, Wallace S, Schwarten D. Transcatheter occlusion of the gastroduodenal artery. Radiology 1979;131:59-64. 13. Stallwood GR, Richards TA. Arteriovenous malformation of the duodenum. Can J Surg 1980;23:572-4. 14. Goff WB, Rosenkrantz H, Healy JF. Angiographic demonstration of bleeding duodenal arteriovenous malformation. J Am Osteopath Assoc 1982;82:189-91. 15. Fowler DL, Fortin D, Wood WG, Pinkerton JA Jr, Koontz PG Jr. Intestinal vascular malformations. Surgery 1979;86:377-85. GASTROINTESTINAL ENDOSCOPY
103
16. Criando KJ, Shureigh SF, Howard WH, Wilson TH Jr. Arteriovenous malformations of the duodenum: a report of three cases. Md State Med J 1982;31:63-5. 17. Fujikawa T, Kurata M, Takaori K, Matsusue S, Takeda H, Sakai S. Solitary cavernous hemangioma of the duodenum: report of a case. Surg Today 1996;26:807-9. 18. Rutgeerts P, Vantrappen G, D’Heygere F, Broeckaert L. Transendoscopic Doppler ultrasound: usefulness for diagnosis and treatment of vascular malformations. Endoscopy 1988;20:99-101. 19. Labenz J, Borsch G. Successful endoscopic haemostasis of duodenal variceal bleeding with Histoacryl [letter]. Endoscopy 1993;25:194.
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20. Kok KYY, Kum CK, Goh PMY. Endoscopic hemostasis of upper gastrointestinal bleeding with histoacryl: last resort before surgery. Endoscopy 1996;28:256-8. 21. Takiguchi N, Ichiki N, Ishige H, Yamazaki T, Sarashina H, Suzuki I, et al. Pancreatic arteriovenous malformation involving adjacent duodenum in a patient with gastrointestinal bleeding. Am J Gastroenterol 1995;90:1151-4. 22. Shahrudin MD, Noori SM. Management of a rare case of arteriovenous malformation of the head of the pancreas. Hepatogastroenterology 1997;44:284-7.
VOLUME 52, NO. 1, 2000