Abstract

Case Presentation: A 69-y/o female with a history of congestive heart failure presented with altered mental status, shortness of breath, and nausea. She was found to have acute kidney injury and hyperkalemia. She was admitted to the intensive care unit and underwent emergent dialysis. On third day of admission she complained of vague abdominal pain and nausea. She was pale, tachycardic and abdominal exam revealed a distended abdomen. Her hemoglobin was 6.0 gm/dl and hematocrit was 18%. She became hypotensive requiring three vasopressors. CT abdomen with contrast showed active extravasation at the GE junction and a distended stomach with hypodense material (Figure 1). Following nasogastric aspirate, upper endoscopy revealed active arterial bleeding near the GE junction. A large amount of blood and clot obscured visualization of the underlying lesion. Tamponade was temporarily achieved by insertion of an SB tube and inflation of the gastric balloon. She was transported to Interventional Radiology and underwent left gastric artery embolization. Patient rebled next day. Repeat endoscopy showed evidence of persistent bleeding with a large amount of fresh and old blood in the gastric fundus. The SB tube was reinserted, the gastric balloon inflated and the patient was taken back to Interventional Radiology. Angiography showed evidence of active bleeding from the inferior phrenic artery (Figure 2). This was treated successfully with embolization. Over the next few days her transfusion requirement improved. Repeat upper endoscopy performed on day two following the second embolization showed less amount of old blood in the gastric fundus. The patient's subsequent recovery was uneventful.Figure 1Figure 2Discussion: DLs generally cause brisk arterial bleeding that is identified endoscopically by densely adherent clots with minimal mucosal defect or completely normal underlying mucosa. The proximal stomach is the most common site of DLs, predominantly along the lesser curvature within 5 cm of the gastro-esophageal junction. Our patient was unusual in that, this area was supplied by both the left gastric artery and a branch of the left inferior phrenic artery. Endoscopic hemostasis, when possible, is the modality of choice for the initial treatment of DLs. Angiographic embolization is an alternate modality in patients with active bleeding not amenable to endoscopic therapy. Conclusion: Dieulafoy's lesion is a potentially life-threatening cause of upper gastrointestinal hemorrhage. Diagnosis is often problematic. Our patient's catastrophic hemorrhage secondary to DL required both endoscopic and angiographic modalities to achieve hemostasis.

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