S2797 First Case of Isolated Angioedema of the Bowel Caused by Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

Abstract

INTRODUCTION: Visceral angioedema (VA) has been widely reported as a side-effect of angiotensin-converting enzyme inhibitors (ACEI). We report the first case of VA from NSAIDs. CASE DESCRIPTION/METHODS: An 80 y/o F with history of multiple abdominal surgeries, hypertension on lisinopril, and lumbago on aspirin 325 mg twice daily presented with acute epigastric pain, nausea, and vomiting. A CT scan showed moderate thickening and dilation of the distal small bowel (SB), without transition point. Symptoms resolved within days with supportive measures. One month later, while asymptomatic, a non-contrast MRI for pancreatic cyst surveillance showed normal SB. Two weeks after the MRI, her abdominal symptoms recurred. CT scan revealed multiple dilated, edematous fluid-filled stretches of SB, without transition point. Symptoms resolved spontaneously within days. Two months later, symptoms returned, with CT showing similar edema in the colon wall (Figure 1). Due to sharp angulations from edematous bowel, only a gastroscope could traverse the colon, with normal appearance of mucosa from the anus to the hepatic flexure. No SB evaluation was attempted due to SB edema. She improved after conservative management. She discontinued her lisinopril. One month later, symptoms recurred, with CT scan showing worsened bowel wall edema from prior CT (Figure 2). Labs were unremarkable for serum complement C4, C1 esterase inhibitor functional assay, extended stool pathogen panel, complete blood count, monoclonal gammopathy screen, and serum cytomegalovirus DNA. Aspirin was stopped. Symptoms abated within 24 hours. Five weeks later, while asymptomatic, her CT showed normalization of bowel wall (Figure 3). In no episode did the patient experience constitutional symptoms, dermatologic changes, dyspnea/wheezing, diarrhea, melena, or hematochezia. She had no new exposure to medications, travel, or dietary changes. In all cases where intravenous contrast was used, splanchnic vessels were patent. DISCUSSION: Episodic bowel obstructive symptoms associated with bowel thickening—and interval clinical improvement paralleling radiologic improvement of bowel thickening—illustrate the cadence of VA. As the VA occurred one month after stopping her ACEI, and symptoms resolved after stopping NSAIDs, it was likely triggered by her NSAID use. The shared pathogenesis and presentation of angioedema and enteropathy caused by NSAIDs provide a rationale for NSAID-induced VA. In patients without resolution of VA after stopping ACEI, NSAID cessation is the next step.Figure 1.: Computed tomography scan of the abdomen with intravenous contrast showed diffuse wall thickening of the descending and rectosigmoid colon. No transition point observed. Wall thickening, edema, and increased mucosal enhancement of multiple loops of the ileum and distal jejunum were observed, as well.Figure 2.: Computed tomography scan of the abdomen with intravenous contrast showed worsened evaluation compared to the previous scan. Diffuse wall thickening of the descending and rectosigmoid colon can be seen. No transition point can be seen. Wall thickening, edema, and increased mucosal enhancement of multiple loops of the ileum and distal jejunum were observed as well.Figure 3.: Five weeks after discontinuing her twice-daily aspirin, the patient underwent computed tomography scan with oral contrast (no intravenous contrast used), which showed interval resolution of the small bowel and colon wall thickening.