Abstract
In general, angioedema can be caused by a hereditary C1 esterase deficiency or by an allergy-related cascade involving either a histamine or a bradykinin-induced cascade. Angioedema secondary to angiotensin-converting enzyme inhibitors (ACEi) typically induces an allergy-related angioedema and typically presents complications associated with the upper airway, and rarely presents intra-abdominally. This case discussed how a 54-year-old male with a recent diagnosis of hypertension presented with acute abdominal pain. He was started on a lisinopril-hydrochlorothiazide combination two days before the presentation. Differentials were considered for an acute abdomen, and a CT abdomen was obtained, which was significant for the thickening of the jejunum and sigmoid colon with surrounding mucosal edema and inflammatory changes. The patient was ultimately treated for bowel angioedema successfully with dexamethasone, diphenhydramine, and famotidine, and his lisinopril was discontinued. This case report aims to discuss and evaluate bowel angioedema in the setting of ACEi use and how it should be considered as a differential for an acute abdomen and its relevant empirical management with steroids due to the indistinguishable etiology of histamine or bradykinin mediated.