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Endoscopic duodenal variceal ligation: a series of 4 cases and review of the literature (with video)
Endoscopic duodenal variceal ligation: a series of 4 cases and review of the literature (with video) A. Clark Gunnerson, DO,2 David L. Diehl, MD, FACP, FASGE,1 Viet-Nhan H. Nguyen, DO,1 Matthew J. Shellenberger, DO,1 Joseph Blansfield, MD3 Danville, Pennsylvania, USA
Ectopic GI varices are rare, and of these, the most common location of bleeding is in the duodenum. Duodenal varices are most commonly caused by portal hypertension secondary to cirrhosis, but there may be other etiologies. The rarity of cases has made determining the best method of treatment difficult, and the medical literature lacks information regarding long-term treatment outcomes. We have encountered 4 cases of duodenal varices of varying etiologies managed with endoscopic variceal ligation (EVL). We summarize the results of EVL in these cases and review the literature regarding EVL for treatment of duodenal varices.
CASES Case 1 A 49-year-old man with alcoholic cirrhosis was admitted with hematemesis and hematochezia. His hemoglobin was 5.0 g/dL, requiring multiple blood transfusions. At another hospital he underwent EGD and colonoscopy (two each) and mesenteric angiography without any source of bleeding found. He was transferred to our hospital with hypotension requiring 2 vasopressors. EGD showed grade I esophageal varices and a single duodenal varix with a red spot. A transjugular intrahepatic portosystemic shunt (TIPS) was placed, with a resulting portosystemic gradient of 12 mm Hg. However, recurrent bleeding occurred 2 days later. EGD again demonstrated the duodenal varix with a “divot,” and a single band was placed on the varix. The patient became hemodynamically stable, did not rebleed, and was able to be weaned off of the
Abbreviations: EVL, endoscopic variceal ligation; TIPS, transjugular intrahepatic portosystemic shunt. DISCLOSURE: All authors disclosed no financial relationships relevant to this publication. Copyright © 2012 by the American Society for Gastrointestinal Endoscopy 0016-5107/$36.00 http://dx.doi.org/10.1016/j.gie.2012.05.020 Received March 24, 2012. Accepted May 14, 2012. Current affiliations: Department of Gastroenterology and Nutrition (1), Department of Internal Medicine (2), Department of Surgery (3), Geisinger Medical Center, Danville, Pennsylvania, USA. Reprint requests: David L. Diehl, MD, Department of Gastroenterology and Nutrition, Geisinger Medical Center, 100 N. Academy Ave, 21-11, Danville, PA 17822.
900 GASTROINTESTINAL ENDOSCOPY Volume 76, No. 4 : 2012
vasopressors. He died a week later, however, because of multiple-organ failure.
Case 2 A 50-year-old man was admitted to another hospital with several episodes of melena and hematochezia. He had a history of a work-related abdominal crush injury 25 years earlier, which had resulted in a partial hepatectomy and splenectomy. EGD showed a medium-sized submucosal mass in the second portion of the duodenum, with central umbilication and fresh blood in the lumen. The endoscopic impression was that the lesion was a GI stromal tumor with ulceration. The patient was transferred to our hospital, and EUS demonstrated the mass to be a varix (Fig. 1). CT angiogram demonstrated an atrophic and calcified inferior vena cava with numerous collateral vessels throughout the abdomen and pelvis, one of which involved the second portion of the duodenum. EGD was done with application of 3 bands to the large varix, with no further bleeding. Follow-up EUS 4 weeks later showed resolution of the duodenal varix. The patient has had no further episodes of bleeding over 2 years of follow-up.
Case 3 A 61-year-old woman was admitted to another hospital with generalized weakness and intermittent melena during the preceding 3 months, requiring more than 30 units of blood. Despite endoscopic evaluation, no bleeding source was found. The patient was transferred to this hospital, and EGD showed varices in the second portion of the duodenum with stigmata of recent bleeding. CT confirmed varices in the second and third portions of the duodenum, which drained into the inferior vena cava, probably through the right gonadal vein. A transjugular liver biopsy with portosystemic pressure measurements showed steatosis but no cirrhosis and a gradient of 8 mm Hg. Angioembolization of a tributary off of the distal right gonadal vein was done, but bleeding continued. Repeat EGD showed 3 varices in the second portion of the duodenum, one with a red wale sign (Fig. 2 and Video). These were treated successfully by using 3 bands, with no further bleeding. Additional banding was done 6 and 10 weeks after the first session, at which time no further varices were seen. Eight months later, the patient was readmitted for melena and hematochezia. EGD showed a single duodenal varix, which was banded. Six weeks later, the patient www.giejournal.org
Gunnerson et al
Endoscopic duodenal variceal ligation
Figure 1. (Case 2): A, CT shows collateral veins in the approximate location of the inferior vena cava, which was injured in an accident years before. One of these involves the second portion of the duodenum (arrow). B, EGD demonstrates a varix in the second portion of the duodenum, with an ulcer on the distal edge (arrow). C, EUS confirms a single tubular anechoic Doppler-positive structure consistent with a varix. D, Post-banding appearance.
returned with bleeding, and EGD showed a scarred down, non-bleeding, duodenal varix with stigmata of recent bleeding. Banding was attempted, but submucosal fibrosis prevented the varix from being suctioned into the cap. Therefore, injection sclerotherapy was done with 6 mL of sodium morrhuate. The patient had mild abdominal pain after the procedure, and a CT scan showed a focal duodenal perforation with periduodenal air, which resolved with conservative management. The CT also showed large periduodenal veins, which appeared to communicate with the inferior vena cava and superior mesenteric vein. An elective exploratory laparotomy was done 3 weeks later, with ligation of the duodenal varices. The patient has had no further bleeding through 9 months of follow-up. www.giejournal.org
Case 4 A 57-year-old man with cirrhosis related to hepatitis C and alcohol use had a TIPS procedure 1 year previously for multiple episodes of bleeding from gastric and duodenal varices. He was admitted with hematochezia and melena. An EGD showed non-bleeding varices in the second portion of the duodenum. US showed a thrombosed TIPS; however, attempted revision was unsuccessful. Hematochezia continued, and another EGD showed numerous varices in the second and third portions of the duodenum. Red wale signs were present, and 2 bands were placed, with successful hemostasis. An EGD was repeated 1 week later, and 4 more bands were placed on other varices. Another EGD was performed 1 month later, and 3 more Volume 76, No. 4 : 2012 GASTROINTESTINAL ENDOSCOPY 901
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Figure 2. (Case 3): A, CT shows an anomalous vein in the descending and horizontal portions of the duodenum, which appears to communicate with the right gonadal vein. B, EGD demonstrates complex duodenal varices and a visible ulcer on the surface of one. C, After placement of 3 bands. D, Mucosal scars from multiple prior banding procedures are seen 4 months later.
bands were placed but with incomplete eradication of the duodenal varices. Follow-up EGD 3 weeks later showed multiple varices in the third and fourth portions of the duodenum, which appeared to be increasing in size and number. For this reason, no banding was done. The patient has not had further bleeding over 9 months of close clinical follow-up.
DISCUSSION Duodenal varices were first demonstrated by radiographic findings in 3 cases by Alberti in 1931.1 Currently, duodenal varices are most commonly identified by upper 902 GASTROINTESTINAL ENDOSCOPY Volume 76, No. 4 : 2012
endoscopy, CT, or mesenteric angiography. On occasion, they are discovered only after exploratory surgery for a bleeding duodenal lesion. Duodenal varices are typically located in the first or second portions of the duodenum, but more distal varices also can occur. The anatomy of duodenal varices generally consists of single afferent and efferent vessels. This differs from esophageal varices, which can be fused with numerous superficial and deep submucosal veins. The afferent vessel of duodenal varices is usually the pyloric, cystic, or superior/inferior pancreaticoduodenal vein originating from the portal vein trunk or the superior mesenteric vein. The efferent vessel then drains into the inferior vena cava directly or through retroperitoneal veins.2 www.giejournal.org
Gunnerson et al
Endoscopic duodenal variceal ligation
TABLE 1. Patient characteristics and treatment
Esophageal or gastric varices
Previous treatment
DVL sessions (total bands)
Age, y
Sex
Liver disease
1
49
M
Cirrhosis, acute alcoholic hepatitis
Cirrhosis
12
Yes
No
1 (1)
Hemostasis achieved with EVL; death from multiple-organ failure related to liver disease 8 d later.
2
50
M
Chronic hepatitis C, bridging fibrosis but not cirrhotic
Inferior vena cava injury
6
No
No
1 (3)
Complete ablation of duodenal varix proven by EUS; no further bleeding at 18 mo follow-up.
3
61
F
Non-cirrhotic
Anomalous periduodenal veins, abnormal right gonadal vein
8
No
IR embolization
4 (6)
Stable for 9 mo after EVL; recurrent bleeding led to 1 EVL then 1 sclerotherapy; surgery eventually done 1 year after banding started.
4
57
M
Cirrhosis
Cirrhosis
15
Yes
TIPS ⫻ 2
3 (9)
Inability to eradicate after 3 sessions; has not bled over last 8 mo.
Case
Cause of duodenal varices
Portal systemic gradient (mm Hg)
Outcome
EVL, Endoscopic variceal ligation; TIPS, transjugular intrahepatic portosystemic shunt.
Duodenal varices can occur in conjunction with esophageal and/or gastric varices, or they may be isolated. It is possible that they may arise after eradication of esophageal or gastric varices. Matsui et al3 identified 12 patients with duodenal varices, 10 of whom also had esophageal and/or gastric varices. Five patients required treatment because of bleeding duodenal varices, 3 of whom had received prior treatment for esophageal varices and 1 for duodenal varices. Most cases of duodenal varices occur secondary to portal hypertension. Cirrhosis, portal vein obstruction, and splenic vein obstruction are the most common causes.4 An extrahepatic cause of portal hypertension seems to place a patient at greater risk for developing duodenal varices than an intrahepatic cause and may suggest a different pathophysiology for their development.5 In this series (Table 1), 2 of the patients did not have portal hypertension. In case 2, an abdominal crush injury caused inferior vena cava damage and led to expansion of periduodenal venous collateral vessels. In case 3, surgical exploration showed several large periduodenal veins draining into the inferior vena cava. No cause for this unusual anatomy could be found. Wheeler and Warren6 reported the first treatment of bleeding duodenal varices in 1957 in a case of portal hypertension. Hemostasis of the variceal hemorrhage was achieved via suture ligation. Other described surgical treatments include direct varix resection, duodenal resection, or portocaval shunting. One report found that, of www.giejournal.org
these, surgical portosystemic shunting had the best success, whereas direct variceal ligation or resection had poor results, including rebleeding and death.7 Interventional radiology procedures have been used, including embolization, TIPS, and balloon-occluded retrograde transvenous obliteration.8 There are a limited number of reports of endoscopic therapy of bleeding duodenal varices, and these generally have used injection sclerotherapy or rubber band ligation. Endoscopic injection sclerotherapy has shown mixed success and can be complicated by tissue damage, mucosal ulceration, and possibly perforation.9 The use of endoscopic band ligation for the treatment of duodenal varices was first described by Tazawa et al10 in 1995 in a patient with portal hypertension secondary to alcoholic liver disease. An extensive literature review from 1995 to the present found only 15 previously reported cases of duodenal varices treated with EVL.3,8-19 Of these, 13 were treated with banding alone, 1 had banding with injection sclerotherapy, and 1 had banding with partial splenic embolization and injection sclerotherapy. When these cases are combined with our 4 cases, the success of duodenal EVL is significant in that only 3 of 19 patients (15.8%) rebled after treatment, and no deaths occurred because of complications of the procedure or by rebleeding. In 2 patients with rebleeding (at 1 and 5 days), a second attempt at banding the varices (one combined with sclerotherapy) resulted in complete hemostasis without any further rebleeding on follow-up at 11 and 18 Volume 76, No. 4 : 2012 GASTROINTESTINAL ENDOSCOPY 903
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months. In case 3, rebleeding occurred after 3 initially successful banding procedures, and the patient eventually required surgery because it was clear that eradication could not be achieved. Two of the 19 patients (including our first case) died within a week after treatment secondary to complications of liver failure and not related to the variceal treatment. Two other cases had no follow-up mentioned. Of the remaining 15 cases, follow-up periods ranged from 12 days to 78 months. We had excellent initial hemostasis by EVL in all 4 cases. The initial bleeding lesion looked remarkably similar in all cases, specifically a mucosal defect resembling an ulcer on the varix. Red wale signs were seen in 2 cases. However, long-term follow-up showed complete eradication of the duodenal varices in only 1 of the 4 cases. Case 2 had complete eradication after 1 treatment and was free of any further bleeding on endoscopic surveillance 1.5 years later. Case 4 had failure of eradication after 3 banding sessions, but the patient has not had further bleeding over a 9-month follow-up period. There is theoretically an increased risk of complication of banding and sclerotherapy in the duodenum because of the thinness of the wall of this organ. In our 4 cases, there were no complications related to band application of 19 bands in 9 banding sessions. In case 3, four previous EVL sessions led to failure of lifting of the duodenal varix into the suction cap of the multiband ligator. Bleeding was induced by these attempts, and salvage sclerotherapy with sodium morrhuate was done. This led to a small contained perforation that could be managed conservatively. However, it did make the subsequent surgery more difficult because of adhesions in the area. There is a single report of occlusion of the ampulla of Vater,19 which suggests that the endoscopist must be oriented to the duodenal landmarks before banding. In summary, duodenal EVL has a high initial hemostasis rate. Recurrence of duodenal varices after initial eradication may occur and may be treated successfully with repeat endoscopic management in some cases. Duodenal EVL does appear to be safe with no complications in this series and few noted in the literature. Certain cases may be refractory to banding because of the anatomy of the duodenal varices. Long-term eradication is variable and may depend on the cause and extensiveness of the ectopic varices.
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REFERENCES 1. Alberti W. U¨ber den röntgenologischen Nachweis von Varizen in Bulbus duodeni [German]. Fortschr Geb Röntgenstr 1931;43:60-5. 2. Hashizume M, Tanoue K, Ohta M, et al. Vascular anatomy of duodenal varices: angiographic and histopathological assessments. Am J Gastroenterol 1993;88:1942-5. 3. Matsui S, Kudo M, Ichikawa T, et al. The clinical characteristics, endoscopic treatment, and prognosis for patients presenting with duodenal varices. Hepatogastroenterology 2008;55:959-62. 4. Tanaka T, Kato K, Taniguchi T, et al. A case of ruptured duodenal varices and review of the literature. Jpn J Surg 1988;18:595-600. 5. Linder S, Wiechel KL. Duodenal varicose veins. Surg Endosc 1991;5:31-5. 6. Wheeler HB, Warren R. Duodenal varices due to portal hypertension from arteriovenous aneurysm: report of a case. Ann Surg 1957;146: 229-38. 7. Khouqeer F, Morrow C, Jordan P. Duodenal varices as a cause of massive upper gastrointestinal bleeding. Surgery 1987;102:548-52. 8. Haruta I, Isobe Y, Ueno E, et al. Balloon-occluded retrograde transvenous obliteration (BRTO), a promising nonsurgical therapy for ectopic varices: a case report of successful treatment of duodenal varices by BRTO. Am J Gastroenterol 1996;91:2594-7. 9. Bosch A, Marsano L, Varilek GW. Successful obliteration of duodenal varices after endoscopic ligation. Dig Dis Sci 2003;48:1809-12. 10. Tazawa J, Sakai Y, Koizumi K, et al. Endoscopic ligation for ruptured duodenal varices. Am J Gastroenterol 1995;90:677-8. 11. Fayad N, Nammour F, Elfant A. Endoscopic variceal ligation for bleeding duodenal varices. J Clin Gastroenterol 2004;38:467. 12. Goetz M, Rahman FK, Galle PR, et al. Duodenal and rectal varices as a source of severe upper and lower gastrointestinal bleeding. Endoscopy 2009;41:E169. 13. Kawakami Y, Takahashi H, Kato S, et al. Effective treatment for duodenal variceal bleeding using endoscopic ligation. Hepatogastroenterology 2011;58:2024-5. 14. Omata F, Itoh T, Shibayama Y, et al. Duodenal variceal bleeding treated with a combination of endoscopic ligation and sclerotherapy. Endoscopy 1998;30:S62-3. 15. Schmeltzer PA, Smith MT. Duodenal variceal bleeding successfully treated with endoscopic banding (with video). Gastrointest Endosc 2011;74:716-7. 16. Shiraishi M, Hiroyasu S, Higa T, et al. Successful management of ruptured duodenal varices by means of endoscopic variceal ligation: report of a case. Gastrointest Endosc 1999;49:255-7. 17. Tan NC, Ibrahim S, Tay KH. Successful management of a bleeding duodenal varix by endoscopic banding. Singapore Med J 2005;46:723-5. 18. Yeh YY, Hou MC, Lin HC, et al. Case report: successful obliteration of a bleeding duodenal varix using endoscopic ligation. J Gastroenterol Hepatol 1998;13:591-3. 19. Silberzweig JE, Atillasoy EO, Sheiner PA, et al. Biliary obstruction caused by endoscopic band ligation of a duodenal varix. Am J Gastroenterol 1997;92:1060-2.
www.giejournal.org
Ectopic GI varices are rare, and of these, the most common location of bleeding is in the duodenum. Duodenal varices are most commonly caused by portal hypertension secondary to cirrhosis, but there may be other etiologies. The rarity of cases has made determining the best method of treatment difficult, and the medical literature lacks information regarding long-term treatment outcomes. We have encountered 4 cases of duodenal varices of varying etiologies managed with endoscopic variceal ligation (EVL). We summarize the results of EVL in these cases and review the literature regarding EVL for treatment of duodenal varices.
CASES Case 1 A 49-year-old man with alcoholic cirrhosis was admitted with hematemesis and hematochezia. His hemoglobin was 5.0 g/dL, requiring multiple blood transfusions. At another hospital he underwent EGD and colonoscopy (two each) and mesenteric angiography without any source of bleeding found. He was transferred to our hospital with hypotension requiring 2 vasopressors. EGD showed grade I esophageal varices and a single duodenal varix with a red spot. A transjugular intrahepatic portosystemic shunt (TIPS) was placed, with a resulting portosystemic gradient of 12 mm Hg. However, recurrent bleeding occurred 2 days later. EGD again demonstrated the duodenal varix with a “divot,” and a single band was placed on the varix. The patient became hemodynamically stable, did not rebleed, and was able to be weaned off of the
Abbreviations: EVL, endoscopic variceal ligation; TIPS, transjugular intrahepatic portosystemic shunt. DISCLOSURE: All authors disclosed no financial relationships relevant to this publication. Copyright © 2012 by the American Society for Gastrointestinal Endoscopy 0016-5107/$36.00 http://dx.doi.org/10.1016/j.gie.2012.05.020 Received March 24, 2012. Accepted May 14, 2012. Current affiliations: Department of Gastroenterology and Nutrition (1), Department of Internal Medicine (2), Department of Surgery (3), Geisinger Medical Center, Danville, Pennsylvania, USA. Reprint requests: David L. Diehl, MD, Department of Gastroenterology and Nutrition, Geisinger Medical Center, 100 N. Academy Ave, 21-11, Danville, PA 17822.
900 GASTROINTESTINAL ENDOSCOPY Volume 76, No. 4 : 2012
vasopressors. He died a week later, however, because of multiple-organ failure.
Case 2 A 50-year-old man was admitted to another hospital with several episodes of melena and hematochezia. He had a history of a work-related abdominal crush injury 25 years earlier, which had resulted in a partial hepatectomy and splenectomy. EGD showed a medium-sized submucosal mass in the second portion of the duodenum, with central umbilication and fresh blood in the lumen. The endoscopic impression was that the lesion was a GI stromal tumor with ulceration. The patient was transferred to our hospital, and EUS demonstrated the mass to be a varix (Fig. 1). CT angiogram demonstrated an atrophic and calcified inferior vena cava with numerous collateral vessels throughout the abdomen and pelvis, one of which involved the second portion of the duodenum. EGD was done with application of 3 bands to the large varix, with no further bleeding. Follow-up EUS 4 weeks later showed resolution of the duodenal varix. The patient has had no further episodes of bleeding over 2 years of follow-up.
Case 3 A 61-year-old woman was admitted to another hospital with generalized weakness and intermittent melena during the preceding 3 months, requiring more than 30 units of blood. Despite endoscopic evaluation, no bleeding source was found. The patient was transferred to this hospital, and EGD showed varices in the second portion of the duodenum with stigmata of recent bleeding. CT confirmed varices in the second and third portions of the duodenum, which drained into the inferior vena cava, probably through the right gonadal vein. A transjugular liver biopsy with portosystemic pressure measurements showed steatosis but no cirrhosis and a gradient of 8 mm Hg. Angioembolization of a tributary off of the distal right gonadal vein was done, but bleeding continued. Repeat EGD showed 3 varices in the second portion of the duodenum, one with a red wale sign (Fig. 2 and Video). These were treated successfully by using 3 bands, with no further bleeding. Additional banding was done 6 and 10 weeks after the first session, at which time no further varices were seen. Eight months later, the patient was readmitted for melena and hematochezia. EGD showed a single duodenal varix, which was banded. Six weeks later, the patient www.giejournal.org
Gunnerson et al
Endoscopic duodenal variceal ligation
Figure 1. (Case 2): A, CT shows collateral veins in the approximate location of the inferior vena cava, which was injured in an accident years before. One of these involves the second portion of the duodenum (arrow). B, EGD demonstrates a varix in the second portion of the duodenum, with an ulcer on the distal edge (arrow). C, EUS confirms a single tubular anechoic Doppler-positive structure consistent with a varix. D, Post-banding appearance.
returned with bleeding, and EGD showed a scarred down, non-bleeding, duodenal varix with stigmata of recent bleeding. Banding was attempted, but submucosal fibrosis prevented the varix from being suctioned into the cap. Therefore, injection sclerotherapy was done with 6 mL of sodium morrhuate. The patient had mild abdominal pain after the procedure, and a CT scan showed a focal duodenal perforation with periduodenal air, which resolved with conservative management. The CT also showed large periduodenal veins, which appeared to communicate with the inferior vena cava and superior mesenteric vein. An elective exploratory laparotomy was done 3 weeks later, with ligation of the duodenal varices. The patient has had no further bleeding through 9 months of follow-up. www.giejournal.org
Case 4 A 57-year-old man with cirrhosis related to hepatitis C and alcohol use had a TIPS procedure 1 year previously for multiple episodes of bleeding from gastric and duodenal varices. He was admitted with hematochezia and melena. An EGD showed non-bleeding varices in the second portion of the duodenum. US showed a thrombosed TIPS; however, attempted revision was unsuccessful. Hematochezia continued, and another EGD showed numerous varices in the second and third portions of the duodenum. Red wale signs were present, and 2 bands were placed, with successful hemostasis. An EGD was repeated 1 week later, and 4 more bands were placed on other varices. Another EGD was performed 1 month later, and 3 more Volume 76, No. 4 : 2012 GASTROINTESTINAL ENDOSCOPY 901
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Figure 2. (Case 3): A, CT shows an anomalous vein in the descending and horizontal portions of the duodenum, which appears to communicate with the right gonadal vein. B, EGD demonstrates complex duodenal varices and a visible ulcer on the surface of one. C, After placement of 3 bands. D, Mucosal scars from multiple prior banding procedures are seen 4 months later.
bands were placed but with incomplete eradication of the duodenal varices. Follow-up EGD 3 weeks later showed multiple varices in the third and fourth portions of the duodenum, which appeared to be increasing in size and number. For this reason, no banding was done. The patient has not had further bleeding over 9 months of close clinical follow-up.
DISCUSSION Duodenal varices were first demonstrated by radiographic findings in 3 cases by Alberti in 1931.1 Currently, duodenal varices are most commonly identified by upper 902 GASTROINTESTINAL ENDOSCOPY Volume 76, No. 4 : 2012
endoscopy, CT, or mesenteric angiography. On occasion, they are discovered only after exploratory surgery for a bleeding duodenal lesion. Duodenal varices are typically located in the first or second portions of the duodenum, but more distal varices also can occur. The anatomy of duodenal varices generally consists of single afferent and efferent vessels. This differs from esophageal varices, which can be fused with numerous superficial and deep submucosal veins. The afferent vessel of duodenal varices is usually the pyloric, cystic, or superior/inferior pancreaticoduodenal vein originating from the portal vein trunk or the superior mesenteric vein. The efferent vessel then drains into the inferior vena cava directly or through retroperitoneal veins.2 www.giejournal.org
Gunnerson et al
Endoscopic duodenal variceal ligation
TABLE 1. Patient characteristics and treatment
Esophageal or gastric varices
Previous treatment
DVL sessions (total bands)
Age, y
Sex
Liver disease
1
49
M
Cirrhosis, acute alcoholic hepatitis
Cirrhosis
12
Yes
No
1 (1)
Hemostasis achieved with EVL; death from multiple-organ failure related to liver disease 8 d later.
2
50
M
Chronic hepatitis C, bridging fibrosis but not cirrhotic
Inferior vena cava injury
6
No
No
1 (3)
Complete ablation of duodenal varix proven by EUS; no further bleeding at 18 mo follow-up.
3
61
F
Non-cirrhotic
Anomalous periduodenal veins, abnormal right gonadal vein
8
No
IR embolization
4 (6)
Stable for 9 mo after EVL; recurrent bleeding led to 1 EVL then 1 sclerotherapy; surgery eventually done 1 year after banding started.
4
57
M
Cirrhosis
Cirrhosis
15
Yes
TIPS ⫻ 2
3 (9)
Inability to eradicate after 3 sessions; has not bled over last 8 mo.
Case
Cause of duodenal varices
Portal systemic gradient (mm Hg)
Outcome
EVL, Endoscopic variceal ligation; TIPS, transjugular intrahepatic portosystemic shunt.
Duodenal varices can occur in conjunction with esophageal and/or gastric varices, or they may be isolated. It is possible that they may arise after eradication of esophageal or gastric varices. Matsui et al3 identified 12 patients with duodenal varices, 10 of whom also had esophageal and/or gastric varices. Five patients required treatment because of bleeding duodenal varices, 3 of whom had received prior treatment for esophageal varices and 1 for duodenal varices. Most cases of duodenal varices occur secondary to portal hypertension. Cirrhosis, portal vein obstruction, and splenic vein obstruction are the most common causes.4 An extrahepatic cause of portal hypertension seems to place a patient at greater risk for developing duodenal varices than an intrahepatic cause and may suggest a different pathophysiology for their development.5 In this series (Table 1), 2 of the patients did not have portal hypertension. In case 2, an abdominal crush injury caused inferior vena cava damage and led to expansion of periduodenal venous collateral vessels. In case 3, surgical exploration showed several large periduodenal veins draining into the inferior vena cava. No cause for this unusual anatomy could be found. Wheeler and Warren6 reported the first treatment of bleeding duodenal varices in 1957 in a case of portal hypertension. Hemostasis of the variceal hemorrhage was achieved via suture ligation. Other described surgical treatments include direct varix resection, duodenal resection, or portocaval shunting. One report found that, of www.giejournal.org
these, surgical portosystemic shunting had the best success, whereas direct variceal ligation or resection had poor results, including rebleeding and death.7 Interventional radiology procedures have been used, including embolization, TIPS, and balloon-occluded retrograde transvenous obliteration.8 There are a limited number of reports of endoscopic therapy of bleeding duodenal varices, and these generally have used injection sclerotherapy or rubber band ligation. Endoscopic injection sclerotherapy has shown mixed success and can be complicated by tissue damage, mucosal ulceration, and possibly perforation.9 The use of endoscopic band ligation for the treatment of duodenal varices was first described by Tazawa et al10 in 1995 in a patient with portal hypertension secondary to alcoholic liver disease. An extensive literature review from 1995 to the present found only 15 previously reported cases of duodenal varices treated with EVL.3,8-19 Of these, 13 were treated with banding alone, 1 had banding with injection sclerotherapy, and 1 had banding with partial splenic embolization and injection sclerotherapy. When these cases are combined with our 4 cases, the success of duodenal EVL is significant in that only 3 of 19 patients (15.8%) rebled after treatment, and no deaths occurred because of complications of the procedure or by rebleeding. In 2 patients with rebleeding (at 1 and 5 days), a second attempt at banding the varices (one combined with sclerotherapy) resulted in complete hemostasis without any further rebleeding on follow-up at 11 and 18 Volume 76, No. 4 : 2012 GASTROINTESTINAL ENDOSCOPY 903
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months. In case 3, rebleeding occurred after 3 initially successful banding procedures, and the patient eventually required surgery because it was clear that eradication could not be achieved. Two of the 19 patients (including our first case) died within a week after treatment secondary to complications of liver failure and not related to the variceal treatment. Two other cases had no follow-up mentioned. Of the remaining 15 cases, follow-up periods ranged from 12 days to 78 months. We had excellent initial hemostasis by EVL in all 4 cases. The initial bleeding lesion looked remarkably similar in all cases, specifically a mucosal defect resembling an ulcer on the varix. Red wale signs were seen in 2 cases. However, long-term follow-up showed complete eradication of the duodenal varices in only 1 of the 4 cases. Case 2 had complete eradication after 1 treatment and was free of any further bleeding on endoscopic surveillance 1.5 years later. Case 4 had failure of eradication after 3 banding sessions, but the patient has not had further bleeding over a 9-month follow-up period. There is theoretically an increased risk of complication of banding and sclerotherapy in the duodenum because of the thinness of the wall of this organ. In our 4 cases, there were no complications related to band application of 19 bands in 9 banding sessions. In case 3, four previous EVL sessions led to failure of lifting of the duodenal varix into the suction cap of the multiband ligator. Bleeding was induced by these attempts, and salvage sclerotherapy with sodium morrhuate was done. This led to a small contained perforation that could be managed conservatively. However, it did make the subsequent surgery more difficult because of adhesions in the area. There is a single report of occlusion of the ampulla of Vater,19 which suggests that the endoscopist must be oriented to the duodenal landmarks before banding. In summary, duodenal EVL has a high initial hemostasis rate. Recurrence of duodenal varices after initial eradication may occur and may be treated successfully with repeat endoscopic management in some cases. Duodenal EVL does appear to be safe with no complications in this series and few noted in the literature. Certain cases may be refractory to banding because of the anatomy of the duodenal varices. Long-term eradication is variable and may depend on the cause and extensiveness of the ectopic varices.
904 GASTROINTESTINAL ENDOSCOPY Volume 76, No. 4 : 2012
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