Successful treatment of ruptured duodenal varices with dual balloon-occluded embolotherapy.

Duodenal varices are ectopic portosystemic shunts that do not tend to result in gastrointestinal bleeding. Balloon-occluded retrograde transvenous obliteration is an established treatment for gastric varices. We report a 60-year-old man with melena due to ruptured duodenal varices originating at an inferior pancreaticoduodenal vein; drainage was into a gonadal vein. His ruptured duodenal varices were successfully treated by dual balloon-occluded embolotherapy.

Duodenal varices are a rare complication of portal hypertension (1, 2). Although bleeding is often severe and fatal, no definitive treatment for bleeding duodenal varices has been established (1, 2). Balloon-occluded retrograde transvenous obliteration (BRTO) is an interventional radiological procedure to address gastric varices; it produces hemostasis in patients with duodenal variceal bleeding (1, 2). Although hemolysis, disseminated intravascular coagulation, and pulmonary embolism have been documented as major complications of BRTO, they are rare (1, 2). We report a patient with ruptured duodenal varices originating at an inferior pancreaticoduodenal vein and drainage into the right gonadal vein that was successfully treated by dual balloon-occluded embolotherapy (DOBE).

Case report

The Human Subjects Research Review Board at our institution approved the interventional protocol; patient consent for inclusion in this retrospective study was waived.

This 60-year-old man suffered from chronic hepatitis due to hepatitis C virus infection since undergoing a right hepatic lobectomy for hepatocellular carcinoma 5 months earlier. Blood transfusions, because he had become anemic with melena and abdominal pain starting approximately one week earlier, failed to improve his symptoms. On the day of the procedure hematemesis developed. Laboratory examinations revealed anemia (hemoglobin 4.7 mg/dl); liver function was graded as Child-Pugh B (total bilirubin 1.8 mg/dl, albumin 2.2 g/dl, prothrombin time 52%, ascites).

Contrast-enhanced computed tomography (CT) scans obtained with a 64-row multidetector CT instrument (Brilliance-64, Philips Medical Systems, Best, The Netherlands) revealed duodenal varices fed from the posterior inferior pancreaticoduodenal vein; drainage was into the right gonadal vein. Esophagogastroduodenoscopy detected active bleeding from ruptured duodenal varices. Conservative management with fasting did not improve his progressive anemia and melena, nor did endoscopic injection sclerotherapy (Fig. 1). Prior written informed consent was obtained for angiography and BRTO or dual balloon-occluded embolotherapy (DBOE) and for entry into this study.

Fig. 1

Endoscopic image showing bleeding duodenal varices

A 5-F guiding sheath (Flexor Tuohy-Borst Side-Arm Introducer; Cook, Bloomington, IN, USA) was inserted from the right femoral vein; to assist in placement we used a 0.035-inch diameter torque Radifocus guidewire (Terumo-Clinical Supply Co., Tokyo, Japan). A 3-F occlusion balloon catheter with an 8-mm diameter balloon (Attendant; Terumo-Clinical Supply Co., Tokyo, Japan) was wedged into the right gonadal vein to introduce a Syncro 2 guidewire (outside diameter 0.014 inch) with a free transformation tip (Boston Scientific Corp., Watertown, MA, USA). We manually injected 10 mL of iomeprol (Iopamiron 300 [300 mg I/mL]; Bayer, Osaka, Japan), inflated the balloon, and obtained right gonadal venography. No opacified duodenal varices were detected (Fig. 2). Subsequently, we used the percutaneous transhepatic approach to insert a 7-F vascular sheath (Medikit Co. Ltd., Tokyo, Japan) and a 5-Fr balloon catheter (Terumo-Clinical Supply Co.) into the posterior inferior pancreaticoduodenal vein. Venography revealed well-opacified duodenal varices (Fig. 3).

Fig. 2

Venographs of the right gonadal vein obtained with an inflated balloon catheter revealed no opacification of the duodenal varices

Fig. 3

Venographs of the right gonadal- and posterior inferior pancreaticoduodenal vein obtained with an inflated balloon catheter revealed well-opacified duodenal varices

We then injected 10 mL of a 70% glucose solution into the gastric varices before injecting 5% ethanolamine oleate (EO) (Odamin; Mochida Pharmaceutical, Tokyo, Japan). The sclerosing agent was a mixture of 10% EO and the same dose of a non-ionic contrast medium (Iopamiron 300) (EOI); this yielded radio-opacity. To prevent hemolysis and subsequent renal failure (3) during the procedure we intravenously delivered 4000 units of human haptoglobin (Green Cross, Osaka, Japan); 1 unit binds 1 mg of hemoglobin. The sclerosing agent was injected slowly under fluoroscopic monitoring until the duodenal varices were completely filled. The injected 5% EOI remained in the varices for 1 h during balloon occlusion. During DOBE we monitored his blood pressure, pulse rate, urine volume, arterial oxygen saturation status (pulse oximeter), and obtained electrocardiograms. We terminated DOBE after 1 h; at that time, test injection of contrast medium showed clot formation in the varices. Lastly a portography was performed. As it revealed marked dilation of the coronary vein compared to pre-DOBE findings we performed microcoil-embolization of this vessel using interlocking detachable coils (Boston Scientific).

After the procedure his hematemesis improved and the hemoglobin increased from 3.6 to 9.7 mg/dl. Esophagogastroduodenoscopy 1 week post-DOBE detected no active bleeding from duodenal varices. On endoscopic images there was a change in the color tone (Fig. 4). Although he died from hepatic failure 2 months later, there was no hemorrhage and the hemoglobin did not decrease during that period.

Fig. 4

Endoscopic image obtained 1 week after DOBE reveals the cessation of active bleeding from duodenal varices and a change in the color tone

Discussion

Ectopic varices are large portosystemic venous collaterals that can arise at different sites such as the gastric fundus, body and antrum of the stomach, duodenum, intra- and extrahepatic biliary tree, adjacent to surgically created enteric stoma, small bowel, colon, anorectum, intra-peritoneum, vesicle, and vagina, but not the cardia and esophagus (1, 2, 4). Bleeding ectopic varices account for less than 5% of all variceal hemorrhages (1, 2, 4).

In patients with cirrhosis, surgical procedures are associated with high mortality rates. In emergency endoscopic treatment injection sclerotherapy or variceal ligation is performed to achieve hemostasis (5). However, duodenal varices larger than 15 mm cannot be treated by endoscopic variceal ligation (5). In addition, endoscopic treatment raises the risk of tissue damage, perforation, and progression of bleeding. In our patient, conservative management with fasting did not improve the progressive anemia or melena, and endoscopic injection sclerotherapy also proved unsuccessful.

Interventional radiological therapy is the next step to treat patients with duodenal varices that fail to respond to endoscopic therapy (4). Transjugular intrahepatic portosystemic shunt (TIPS) placement, a less-invasive alternative to portacaval shunt surgery and a hemodynamic equivalent of the side-to-side small-diameter portacaval shunt, reduces the pressure gradient between the portal and systemic circulation. Given the high morbidity and mortality rates of emergency surgical shunt placement in the presence of decompensating cirrhosis, TIPS is a superior option in these patients, even in emergent situations (4). However, even if TIPS can be performed in patients with severe liver dysfunction, it has certain limitations in the presence of severe liver atrophy and carries an increased risk of complications such as hepatic encephalopathy and cerebral embolization (4). Because our patient had undergone right lobectomy for hepatocellular carcinoma 5 months earlier, we considered him ineligible for TIPS.

Hotta et al. (1) reported the successful treatment of duodenal varices with BRTO via the right inferior adrenal vein. In BRTO procedures, the blood flow is blocked by balloon inflation and the injected sclerosing agent induces progressive thrombosis or organization of the variceal lumen. For BRTO to be successful, the draining vein must be identified for appropriate placement of the balloon catheter, and the sclerosing agent must completely fill the varices. In our patient, gonadal venography performed during balloon occlusion showed no opacification of the duodenal varices. Therefore, based on reports describing the successful treatment of gastric varices and hepatic encephalopathy by DOBE (6) we chose to use this technique. CT scans acquired before DOBE revealed duodenal varices; they were fed from the posterior inferior pancreaticoduodenal vein and drained into the right gonadal vein. We introduced balloon catheters via the percutaneous transhepatic approach into the posterior inferior pancreaticoduodenal vein, and used the percutaneous femoral vein approach into the right gonadal vein. The duodenal varices were completely filled by the sclerosing agent.

At BRTO, an EOI mixture or, alternatively, endoscopic injection sclerotherapy is delivered (7). As EO agglutinates platelets and destroys vascular endothelial cells, it functions as a sclerosing agent. However, EO diversion occasionally results in the destruction of red blood cell membranes and complications associated with its use have been reported (7). As Hirota et al. (7) used a 50% glucose solution to reduce the amount of EOI injected into large gastric varices, Ikeda et al. injected a 70% glucose solution and 5% EOI under fluoroscopic monitoring until the duodenal varices were completely filled (8).

Various sclerosants and tissue adhesives have been used for the management of duodenal variceal bleeding. N-butyl-2-cyanoacrylate (NBCA), a tissue adhesive that rapidly polymerizes upon contact with blood and embolizes the varix, has been used to achieve hemostasis in patients with gastrointestinal variceal bleeding (9). It is particularly successful in achieving primary endoscopic hemostasis and is of value as secondary therapy of duodenal varices when other endoscopic approaches have failed (5). However, NBCA injection is not without risks. Reported complications are pulmonary emboli, portal and splenic vein thrombosis, cerebrovascular accidents, recurrent bleeding after cast extrusion, and impaction of the injector needle in the varix (9). This agent is currently not approved for the treatment of varices in the USA and the results obtained with other sclerosants such as ethanolamine oleate, sodium morrhuate, absolute alcohol, and thrombin to achieve hemostasis of duodenal variceal hemorrhage have been mixed (10).

In conclusion, we present a patient whose bleeding duodenal varices were successfully treated by DOBE. There were no major complications during the follow-up period. We suggest that DOBE can be an effective and safe method to treat ruptured duodenal varices in some patients.