Abstract

Editor: A 58-year-old woman with thrombocytopenia (platelet count of 49,000) was admitted for evaluation of high-grade, non-Hodgkin lymphoma. After undergoing chemotherapy, she became pancytopenic and developed recurrent gastrointestinal (GI) bleeding. Her thrombocytopenia was minimally responsive to platelet transfusion because of a consumptive coagulopathy. Management was further complicated by a critical, region-wide platelet shortage; the blood bank had no platelets available. Upper endoscopy revealed bright red blood refluxing back from the descending duodenum, with fresh blood clot over an actively bleeding ulcer. Over the course of 48 hours, two subsequent attempts were unsuccessful in cauterizing the ulcer endoscopically with bicap coagulation and epinephrine injection. The patient presented to the interventional radiology department with life-threatening recurrent upper GI bleeding, and was a poor surgical candidate (hemoglobin, 8.4; hematocrit, 24.5; platelets, 15,000). Selective celiac and gastroduodenal arteriography failed to demonstrate the active bleeding site. However, hyperemia was seen in the postbulbar duodenum. The right gastroepiploic artery was embolized with two helical coils and the gastroduodenal artery (GDA) was embolized with use of Gelfoam pledgets until vascular stasis was achieved. This stabilized the patient for 48 hours, at which point she experienced rebleeding. Repeated endoscopic attempts at cauterization and epinephrine injection failed. Massive packed red blood cell resuscitation was required. Platelets remained at 28,000. Repeated arteriography demonstrated active bleeding in the descending duodenum and recanalization of the GDA. A microcatheter was used to selectively access the feeding vessel in the duodenal wall, where one helical and two straight coils were placed. Repeated arteriography showed a patent vessel with persistent bleeding (Fig 1a). Only six units of platelets were available in the hospital's blood bank at this time. Three units were selectively injected into the bleeding vessel over 10 minutes. Post-transfusion angiography demonstrated interval coagulation with occlusion of the vessel and arresting of bleeding (Fig 1b). Given that multiple attempts at nonsurgical management had failed, the GDA and inferior pancreaticoduodenal artery (IPDA) were embolized with coils. In the presence of platelet shortage, resistant thrombocytopenia, consumptive coagulopathy, or sequestration, selective delivery of platelets with transcatheter transfusion may provide effective hemostasis during embolization. However, embolization alone can achieve hemostasis in the vast majority of patients with serious concomitant diseases in whom endoscopic management of massively bleeding duodenal ulcers fails (1Toyoda H Nakano S Takeda I et al.Transcatheter arterial embolization for massive bleeding from duodenal ulcers not controlled by endoscopic hemostasis.Endoscopy. 1995; 27: 304-307Crossref PubMed Scopus (94) Google Scholar). Synchronous embolization of the GDA and IPDA can control persistent duodenal bleeding after failed endoscopic treatment in poor surgical candidates. However, this aggressive therapy should be done only as a life-saving measure because of the risk of duodenal and pancreatic necrosis (2Bell S Ying Lau K Sniderman K Synchronous embolization of the gastroduodenal artery and the inferior pancreaticoduodenal artery in patients with massive duodenal hemorrhage.J Vasc Interv Radiol. 1995; 6: 531-536Abstract Full Text PDF PubMed Scopus (28) Google Scholar).

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