Case Presentation: A 42-year-old African woman with past medical history of anxiety, depression, hyperlipidemia and recent diagnosis of hypertension presented with two days of acute onset, severe, persistent, cramping mid-epigastric abdominal pain worse with eating and drinking. The pain was associated with nausea and non-bloody non-bilious emesis. The patient was initiated on lisinopril-hydrochlorothiazide two days prior to onset of symptoms for hypertension. Vital signs on admission were normal. The patient had tenderness throughout the abdomen, worst over the epigastric region. Complete blood count and complete metabolic panels were unremarkable. Serum lipase and stool studies were unremarkable. Computed Tomography (CT) scan of the abdomen and pelvis with contrast revealed thick-walled jejunum consistent with angioedema. The patient underwent an esophagogastroduodenoscopy which showed mild gastritis. Lisinopril was discontinued and patient’s diet was advanced over the subsequent 1-2 days. Repeat CT scan revealed that the previously noted jejunal wall thickening had resolved completely. The patient was discharged with the knowledge that she is to avoid ACE inhibitors in the future.
Discussion: Lisinopril is an angiotensin converting enzyme (ACE) inhibitor commonly prescribed for high blood pressure and other cardiovascular conditions. Angioedema is a known side effect of ACE inhibitors (1). There have only been a handful of case reports that describe angioedema of the small bowel due to ACE inhibitors (2); furthermore, the angioedema described in these case reports has been limited to the ileum (3). Here, we present a rare case of isolated jejunal edema in the setting of recent ACE inhibitor therapy initiation. Angioedema occurs in the skin and mucous membranes and is due to vasodilation which leads to serum accumulation in interstitial tissue spaces. ACE inhibitor induced angioedema is estimated to occur in approximately 0.1-0.5% of patients receiving these medications although it may be underrecognized (4). Although the mechanism is not entirely understood, one explanation is that ACE inhibitors induce angioedema due to elevated levels of bradykinin (5). Clinical symptoms of intestinal angioedema include abdominal pain, nausea, vomiting and diarrhea (4). Abdominal pain can be severe and mistaken for small-bowel obstruction. Recognition of the association between ACE inhibitor and abnormal CT findings suggestive of angioedema can lead to early diagnosis, prevention of invasive measures and improved outcomes for patients.
Conclusions: ACE inhibitors induced angioedema can involve any visceral organ but mostly occurs in the periorbital region, perioral region, tongue, and oropharynx. Patients who present with abdominal pain, nausea, vomiting and/or other gastrointestinal symptoms after initiation of an ACE inhibitor may be experiencing isolated bowel angioedema which can rarely be limited to small bowel only. Symptoms generally improve in 1-2 days after cessation of the medication.