Abstract

Introduction: Gastrointestinal (GI) bleeding is a common cause for hospital admission and rare etiologies can be difficult to identify with conventional diagnostic techniques. Case Description: This is a 67-year-old female who underwent a Whipple procedure for a benign pancreatic cystic mucinous ductal lesion and presented with signs of occult GI bleeding requiring blood transfusions one year later. Prior to this admission, she required monthly hospitalizations and transfusions for recurrent symptomatic anemia. Despite extensive evaluation, no source was identified. During her current hospital admission, she presented with recurrent daily maroon colored stools. She underwent nuclear medicine tagged RBC scan, CT angiogram, colonoscopy, EGD and single balloon endoscopy during her two-week hospital stay but they did not identify a source of bleeding. She required daily blood transfusions to treat her symptomatic anemia. Ultimately, it was hypothesized that reconstruction of her portal vein during her Whipple surgery may have resulted in pre-hepatic portal hypertension. She was started on a trial of octreotide which stabilized her hemoglobin. On follow-up, her symptoms had greatly improved and she required one additional hospitalization since discharge. At 12 months follow-up, octreotide was discontinued successfully and her hemoglobin has remained stable. Discussion: Portal hypertension results from impaired outflow from the portal bed. Pre-hepatic etiologies include portal vein thrombosis, stricture, or invasive tumor affecting the portal vein. Etiology dictates medical and surgical options for therapy and in non-cirrhotic patients, bypassing the liver may not improve portal hypertension. In this case, the patient's history of Whipple surgery resulted in pre-hepatic portal hypertension secondary to manipulation and diffuse damage to the portal vein. Studies have demonstrated long-term management with octreotide reduces portal pressure, sustains reduced pressure for an extended period of time, and reduces formation of collateral flow (1,2).

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