1. Co-existence of Gastrointestinal Vascular Malformations in Patients With Congenital Head/neck and Thoracic Vascular Malformations and Vascular Birthmarks Kshitij Chatterjee, Jagpal S. Klair, Mohit Girotra, Saranya Addepally, Aneet Kaur, Farshad Aduli Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Arkansas for Medical Sciences (UAMS) & Central Arkansas Veterans Health Services (CAVHS), Little Rock, AR INTRODUCTION Vascular malformations are congenital vascular anomalies, which can involve only veins (VMs), lymphatics (LMs), veins and lymphatics (LVMs), or arteries and veins bypassing capillaries (AVMs). In the GI tract, smaller AVMs are well-recognized etiology for both occult and overt GI bleeding. There exist good modalities for endoscopic diagnosis of AVMs. However, there is very limited understanding on associations of GI vascular malformations with similar malformations elsewhere in the body. CASE PRESENTATION A 30-year-old man with history of mediastinal, thoracic and paraspinal (T7-12) venous malformations requiring surgical exploration and sclerotherapy, was found to be anemic to 6.8 g/dl, with MCV of 61 fL and ferritin of 5.9 ng/mL and positive guaiac. He denied any features of overt GI bleeding (OGIB). Computed tomography (CT) scan of abdomen showed diffuse wall thickening in cecum and proximal ascending colon; multiple tortuous blood vessels seen around the thickened bowel loops and splenomegaly (Fig 1), but no bleeding within the chest/abdomen or pelvis. Upper GI endoscopy was unremarkable and colonoscopy revealed large VMs in the rectum, ascending colon, and cecum (Fig 2) Subsequent capsule endoscopy disclosed multiple similar VMs in the terminal ileum also. He underwent right hemicolectomy with re- anastomosis and the pathology from his cecum and colon confirmed VMs. His hemoglobin has been stable since surgery. We plan for a repeat colonoscopy in a year. Sporadic angiodysplasia (AD) is commonly seen in patients >60 years of age, especially those with end stage renal disease, aortic stenosis, and von Willebrand disease (vWD), all excluded in our patient. Moreover, our patient had splenomegaly not attributable to any other systemic vascular malformation syndromes like blue rubber bleb nevus syndrome (BRBNS), Klippel-Trenaunay-Weber syndrome, Maffuci syndrome, and Osler-Weber- Rendu syndrome. Therapeutic modalities depend on degree of bleeding and size & number of lesions. Incidental lesions usually require no treatment. Endoscopic therapy with argon plasma coagulation (APC), band ligation, hemoclip placement, and injection sclerotherapy have been effective in reducing long-term bleeding from these lesions. Pharmacological agents may be considered if lesions are widespread or in a poor surgical candidate, with combination hormonal therapy or octreotide. If localized heavy load of VMs, surgery may be the best option, like in our patient. Future research should be directed towards effective pharmacologic agents with widespread action on systemic and GI vascular malformations. REFERENCES Foutch PG, Rex DK, Lieberman DA. Prevalence and natural history of colonic angiodysplasia among healthy asymptomatic people. The American journal of gastroenterology. 1995;90:564-567 Marwick T, Kerlin P. Angiodysplasia of the upper gastrointestinal tract. Clinical spectrum in 41 cases. Journal of clinical gastroenterology. 1986;8:404-407 Fig 1: CT scan of abdomen (Coronal and axial) showing diffuse wall thickening in cecum and proximal ascending colon; multiple tortuous blood vessels seen around the thickened bowel loops and splenomegaly (coronal). DISCUSSION Vascular anomalies of GI tract are generally classified into three groups - Vascular tumors or angiomas (benign or malignant); anomalies associated with systemic or hereditary syndromes; and sporadic lesions. Fig 2: Colonoscopy revealed large VMs in the rectum, ascending colon, and cecum.