Abstract

Introduction: Gastric antral vascular ectasia, or GAVE, is an extremely uncommon cause of recurrent intestinal blood loss. Up to 30% of patients suffering from this type abnormal gastric vasculature also have concurrent cirrhosis. In this case, we describe a patient with past medical history of multiple hospitalizations for anemia secondary to significant GI bleeds, with findings of cryptogenic cirrhosis, severe gastric antral vascular ectasia, splenorenal varices, multiple AVMs of the small bowel, and cavernous hemangiomas. Methods: Our case discusses a 74-year-old female with significant cardiovascular disease (coronary artery disease status post CABG, systolic cardiomyopathy, diabetes, hypertension) and chronic anemia with recurrent GI bleeding, who was admitted to our facility with the chief complaint of increasing lethargy. The patient had been hospitalized on multiple occasions in the past for symptomatic anemia and had required numerous blood transfusions secondary to substantial gastrointestinal blood loss. During this admission, the patient’s hemoglobin was as low as 5.3, with multiple potential sources for a GI bleed. A capsule endoscopy performed 1.5 years prior to this admission revealed evidence of vascular ectasias in the small bowel. A gastroscopy performed 7 months prior and repeated 3 months afterward demonstrated multiple, hemorrhagic, gastric antral vascular ectasias. Colonoscopy performed 2 months prior to admission demonstrated multiple colonic polyps in the cecum and sigmoid colon with pathology revealing a cavernous hemangioma. Results: Upon further investigation of the etiology of her abnormal vasculature, she was found to have evidence of cirrhosis, splenorenal varices, and ascites on CT imaging. Interestingly, however, portal venogram demonstrated no evidence of portal hypertension, and venous duplex confirmed patent portal and splenic veins, ruling out thrombosis. After an exhaustive work-up to determine the source of bleeding, the patient underwent a spiral enteroscopy, which demonstrated actively pumping angio-ectasia within the ileum. She eventually developed a perforated viscus, which required exploratory laparotomy with small bowel resection. Conclusion: This case illustrates the significant GI bleeding caused by a rare case of vascular ectasias in the small bowel. The case also discusses our experience using argon plasma coagulation, electrocautery, and laparoscopic surgery that served as therapeutic options. The pathogenicity of vascular ectasias still remains unclear, and is associated with multiple conditions including cirrhosis, portal hypertension, and cardiovascular disease; however, no direct relationship or etiology has been identified.

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