Angiotensin-Converting Enzyme Inhibitor-Induced Angioedema Following Long-Term Lisinopril Use: Response to C1 Esterase Inhibitor Treatment

Angiotensin-converting enzyme inhibitors (ACEIs) are widely prescribed for cardiovascular and renal conditions, but a rare and potentially life-threatening complication is ACEI-induced angioedema, which results from bradykinin accumulation leading to increased vascular permeability and tissue swelling. This condition may present abruptly, even after years of uneventful therapy, and can threaten the airway. We report the case of an elderly woman in her 80s with hypertension, rheumatoid arthritis, and osteoarthritis, who presented with acute throat and tongue swelling, dysphagia, nausea, and hoarseness after 16 years of lisinopril use. She had no fever, stridor, or rash, but recalled two prior self-limiting episodes of similar swelling. Examination showed pronounced left-sided tongue and submandibular swelling, stable vital signs, and no respiratory distress. Laboratory workup revealed mild anemia and raised CRP, but normal white cell count and organ function. Flexible nasoendoscopy showed arytenoid oedema with a patent airway and normal vocal cord movement. In the absence of urticaria, infection, or allergen exposure, a diagnosis of ACEI-induced angioedema was made. Lisinopril was discontinued, and she received icatibant, intravenous corticosteroids, and antihistamines. Mild oxygen desaturation prompted administration of intravenous C1 esterase inhibitor, which led to rapid improvement. The patient recovered overnight, with resolution confirmed on repeat endoscopy, and was discharged after two days with instructions for alternative antihypertensive management. This case emphasizes that ACEI-induced angioedema can occur unpredictably and may not respond to conventional therapies; however, targeted agents such as icatibant and C1 esterase inhibitors can be effective. Early recognition and multidisciplinary intervention are key to preventing airway compromise in these patients.