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Isolated Laryngeal Angioedema in a Patient with Long-term ACE Inhibitor Use: A Case Report.
Clinical Practice and Cases in Emergency Medicine 2024 Februrary
INTRODUCTION: Angiotensin converting enzyme (ACE) inhibitor-associated angioedema is the most common cause of angioedema seen in the emergency department (ED) and can be associated with a high morbidity. Most cases occur within months of initiation of an ACE inhibitor and are associated with facial and/or oropharyngeal swelling. We present a case of isolated laryngeal edema requiring intubation following 10 years of ACE inhibitor therapy.
CASE REPORT: An 82-year-old female, who was on lisinopril therapy for 10 years, presented to the ED with shortness of breath and a sensation that her throat was swelling. She appeared to be in mild respiratory distress and could only speak in one-word sentences. On the physical exam, there was no swelling in the tongue, lips, or face, and the uvula was midline. There was mild posterior pharyngeal edema and swelling noted, but the airway was not visibly obstructed. She was tachypneic and stridor was present. After no improvement with medications, anesthesia successfully intubated her in the operating room. It was deemed a difficult airway secondary to posterior pharyngeal erythema and edema. She was diagnosed with ACE inhibitor-associated angioedema and was extubated four days later. Her lisinopril was discontinued, and she has not had a recurrence of angioedema.
CONCLUSION: ACE inhibitor-induced angioedema commonly presents with facial and oropharyngeal swelling. Its recognition, even years after starting an ACE inhibitor, is necessary to ensure swift and appropriate treatment of potentially life-threatening posterior pharyngeal edema.
CASE REPORT: An 82-year-old female, who was on lisinopril therapy for 10 years, presented to the ED with shortness of breath and a sensation that her throat was swelling. She appeared to be in mild respiratory distress and could only speak in one-word sentences. On the physical exam, there was no swelling in the tongue, lips, or face, and the uvula was midline. There was mild posterior pharyngeal edema and swelling noted, but the airway was not visibly obstructed. She was tachypneic and stridor was present. After no improvement with medications, anesthesia successfully intubated her in the operating room. It was deemed a difficult airway secondary to posterior pharyngeal erythema and edema. She was diagnosed with ACE inhibitor-associated angioedema and was extubated four days later. Her lisinopril was discontinued, and she has not had a recurrence of angioedema.
CONCLUSION: ACE inhibitor-induced angioedema commonly presents with facial and oropharyngeal swelling. Its recognition, even years after starting an ACE inhibitor, is necessary to ensure swift and appropriate treatment of potentially life-threatening posterior pharyngeal edema.
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