Gastrointestinal: Successful obliteration of bleeding duodenal varices using band ligation

Abstract

A 57 year old male with hepatitis C and alcohol induced cirrhosis, presented to the emergency with hemetemesis and hematochezia, followed by lightheadness and diaphoresis. He had no history of gastrointestinal hemorrhage. The patient was on warfarin and naproxen following recent knee surgery. He continued to drink 2-3 beers daily. On admission, his BP was 96/60 and pulse was 90/min. Physical exam was otherwise unremarkable. Investigations included a hemoglobin of 7.5 g/dl, platelet count 123, BUN of 30, creatinine 0.7, INR of 1.4 and normal liver enzymes. He was resuscitated with blood and IV fluids, and was started on IV esomeprazole and octreotide. An emergent upper endoscopy demonstrated an oozing duodenal varix between the first and the second portion of the duodenum with a platelet plug (Figure 1). Two bands were successfully placed upon the variceal column (Figure 2). No esophageal or gastric varices were identified. The patient had no further bleeding and was discharged several days later. Follow up endoscopy at one month revealed scarring and healing ulceration at the band ligation sites (Figure 3 arrows). Duodenal varix with platelet plug. Duodenal varix immediately post banding. Duodenal varix site one month later. Varices outside the gastro esophageal region, are referred to as ectopic varices. Ectopic varices are rare, and constitute 1 to 5% of all variceal hemorrhage. Nearly 17% of ectopic variceal bleeding occurs in the duodenum. Duodenal varices (DV) in the absence of esophageal varices, as seen in this patient, are an even more uncommon manifestation of portal hypertension. They result from retroperitoneal porto-systemic shunts caused by increased hepatofugal blood flow through the cystic branch of the superior mesenteric vein, superior and inferior pancreaticoduodenal veins, and gastroduodenal and pyloric veins. Such varices are less effective in lowering the portal pressure, compared with esophageal and gastric varices. The serosal and submucosal location of DV, limits visualization during endoscopy. Their clinical significance is not apparent until the varix expands into the submucosal space where it can hemorrhage into the gastrointestinal lumen. Because of the infrequency of DV hemorrhage, treatment modalities have not been prospectively validated. These include surgical intervention (variceal ligation, duodenal resection, and extra-hepatic portosystemic shunt creation), interventional radiological procedures (tranjugular intrahepatic portosystemic shunt, percutaneous transhepatic obliteration, trans-ileocolic vein obliteration, balloon occluded retrograde transvenous obliteration), and endoscopic techniques (band ligation, sclerotherapy and clipping). Contributed by