Life-threatening bleeding from postbulbar duodenal ulcer saved by emergency transcatheter arterial embolization

Abstract

Life-threatening bleeding from postbulbar duodenal ulcer saved by emergency transcatheter arterial embolizationTo the Editor: Immediate operation is the standard procedure to arrest life-threatening bleeding from postbulbar duodenal ulcer (PDU) not amenable to endoscopic treatment. Nonetheless, even in operable cases, mortality and morbidity rates for hemorrhagic PDUs are high. 1,2 Here we report on a patient with lifethreatening hemorrhage from PDU, who, after failed endoscopic treatment, was successfully saved by emergency transcatheter arterial embolization (TAE) with polyvinyl alcohol and gelatin sponge particles.A 69-year-old man underwent a coronary artery bypass graft for myocardial infarction, and was discharged 17 days later. Before and following the procedure, standard-dose histamine receptor antagonist was administered to the patient. Warfarin was given orally (Thrombotest, 10%-20%). Nonsteroidal antiinflammatory drugs (NSAIDs) were not administered. On the next day, the patient presented at our institution unconscious (owing to hypovolemic shock) and with tarry stool. He was stabilized by rapid fluid resuscitation. Upper gastrointestinal endoscopy disclosed multiple, small, shallow ulcers in the postbulbar lesion of the duodenum, with bleeding from one of these ulcers. Hemostatic clips were used to control bleeding at the site (Fig. 1). Nonetheless, the following day, hemorrhage recurred and the patient again went into shock. In this instance, endoscopic treatment was not feasible because hematoma obscured visualization of the bleeding site. Contrast-enhanced computed tomography (CT) images showed an intraluminal extravasation from the anterior wall of the duodenum. Emergency diagnostic angiography revealed extravasation from the duodenal branch arising from the anterior superior pancreaticoduodenal artery (ASPDA) (Fig. 2), and superselective TAE was performed immediately. The feeding branch was embolized using polyvinyl alcohol particles ranging in size from 500 to 700 µm (Ivaron, Contour; Boston Scientific, Fremont, CA, USA), beginning with the ASPDA. To ensure hemostasis, gelatin sponge particles (Gelfoam; Pharmacia and Upjohn, Kalamazoo, MI, USA) were added. Subsequent angiography showed complete occlusion. No increase in serum levels of transaminases or amylase was noted. Improvement of PDUs (including the hemorrhagic ulcer) was achieved with proton pump inhibitor therapy, and duodenal ischemia was not observed. The serum gastrin level, which was elevated (307 pg/ml) before TAE, decreased to 101 pg/ml after the procedure (normal range, 37-172 pg/ml). The patient has been well and without recurrent ulcer formation or bleeding for 50 months.

Nature and treatment outcomes of bleeding post‐bulbar duodenal ulcers

“…[12][13][14][15][16][17][18][19][20][21][22] Since then, few studies have addressed this issue collectively, although there have been some case reports. 30,31 In addition, in some of these studies they were diagnosed in selected patient groups, such as patients who had received surgery. 13,14,19 Hence, the precise, current prevalence of endoscopically-proven PBDU remains obscure.…”

“…Considerable numbers of studies on PBDUs were performed from the 1950s to 1980s, demonstrating that PBDUs are relatively rare, accounting for 5–10% of overall DUs 12–22 . Since then, few studies have addressed this issue collectively, although there have been some case reports 30,31 . In addition, in some of these studies they were diagnosed in selected patient groups, such as patients who had received surgery 13,14,19 .…”

“…First, although rebleeding is not related to the hemostasis method, the level of achievement of each hemostasis procedure may have been insufficient in PBDUs due to technical difficulties in the post‐bulbar area. Second, persistent control of the blood supply by endoscopic hemostasis may have been challenging for bleeding from PBDUs due to the anatomically complex nature of the pancreaticoduodenal artery arcade or occasionally due to the involvement of a semi‐primary artery, such as the cystic artery 31,38 . Third, whereas gastric acid is involved in the etiology of PBDUs, 12,20,35 bile and pancreatic juice are likely to also be involved in the wound healing of PBDUs.…”

“…Second, persistent control of the blood supply by endoscopic hemostasis may have been challenging for bleeding from PBDUs due to the anatomically complex nature of the pancreaticoduodenal artery arcade or occasionally due to the involvement of a semi-primary artery, such as the cystic artery. 31,38 Third, whereas gastric acid is involved in the etiology of PBDUs, 12,20,35 bile and pancreatic juice are likely to also be involved in the wound healing of PBDUs. Thus, although the efficacy of proton pump inhibitors for reducing rebleeding is well recognized in bleeding peptic ulcers, 39 the efficacy may be somewhat limited in bleeding PBDUs due to the coexistence of bile and pancreatic juice in the post-bulbar area.…”