A 42-year-old African American woman with a history of hypertension, morbid obesity, and obstructive sleep apnea presented to the emergency department with a 12-hour history of left-sided abdominal pain, nausea and vomiting. At presentation her medications included hydrochlorothiazide, acetaminophen, ibuprofen, and lisinopril. Her first dose of lisinopril 5mg was 12 hours before the onset of her symptoms. She had never taken an ACE inhibitor (ACEi) or Angiotensin II Receptor Antagonist (ARB) before.
On presentation, she had crampy abdominal pain that radiated to the left side of her abdomen. Her pain was constant and increasing in severity. She also had persistent nausea with one bout of emesis. She had one non-bloody bowel movement of normal caliber within 24-hours of presenting and denied any recent diarrhea, constipation, or recent sick contacts.
Vitals at presentation included a blood pressure of 187/122, pulse of 81, temperature of 36.7 °C, respirations of 20, and an O2 saturation of 100% on room air. Physical exam showed a patient that was uncomfortable and at times sitting up and writhing in bed with her eyes closed. Her abdomen was tender to palpation in the left epigastric area and left mid abdomen, with mild left suprapubic tenderness. She also had hyperactive bowel sounds but no rebound tenderness or guarding.
The patient received IV fluids and nausea medications. The labs showed an unremarkable CBC with a normal C1 esterase. Stool studies were negative for infectious diseases. CT of the abdomen showed segmented target-like enhancement of a dilated loop of ileum with relatively high attenuation ascites (Image 1).
Given her presentation and findings, drug-induced visceral angioedema due to ACEi was suspected. Lisinopril was discontinued and the patient’s abdominal symptoms resolved completely in 48 hours. On follow-up 2 weeks and 8 weeks later, her symptoms had not returned.
Discussion:
Angioedema occurs in 0.1% to 0.77% of patients taking ACE inhibitors. It usually manifests as swelling of the face, tongue, and lips, and in rare cases, the gastrointestinal wall. Angioedema of the face and visceral regions generally occur within the first week of taking an ACE inhibitor, so the timing of onset is similar regardless of body area involved.
A MEDLINE search was done to elucidate key characteristics. 34 individual reports of ACE-inhibitor induced visceral angioedema were found. Signature features to assist in diagnosing ACEi induced intestinal type angioedema are denoted in Image 2.
In this case the patient had many signature findings including a middle aged woman taking an ACEi, African American ethnicity, abdominal pain without infectious findings, CT findings of bowel-wall thickening, normal C1-esterase inhibitor level and resolution of symptoms after cessation of medication. All of these findings in our patient made us confident in our diagnosis of Isolated Intestinal Type Angioedema.
Conclusions:
ACE inhibitor induced visceral angioedema should be considered in the differential diagnosis of abdominal pain. Awareness is important for early suspicion and will help in avoiding delays in diagnosis, unnecessary testing, and considerable morbidity. Signature findings include a middle aged female patient on an ACE inhibitor presenting with abdominal pain without infectious etiologies, and an abdominal CT scan showing small bowel edema. Cessation of all ACE inhibitors and symptomatic treatment leads to resolution of symptoms.