2024 FSA Podium and Poster Abstracts

P075: DELAYED PRESENTATION OF ANGIOEDEMA IN THE POST-ANESTHESIA CARE UNIT: CASE REPORT
Allyson F Tragesser, MD; Brandon M Lopez, MD; David Hutchinson, MD; University of Florida

Introduction/Background: Angioedema, a rare yet potentially life-threatening complication, has been documented in various clinical settings. There are few case reports describing patients who develop severe isolated angioedema in the perioperative setting. We present a unique case of severe asymmetrical angioedema observed in the post-anesthesia care unit (PACU) hours after receiving uneventful general endotracheal anesthesia for a knee operation. The angioedema was likely attributable to chronic Angiotensin Converting Enzyme (ACE) inhibitor use.

Methods: This report details a clinical case of a 65-year-old African American female with a history of hypertension (on amlodipine, hydrochlorothiazide, and lisinopril), coronary artery disease with previous stents in 2016, and osteoarthritis. This patient underwent multiple prior surgeries without anesthesia complications. The patient presented for left knee hardware removal. Intraoperatively, the patient had an uneventful course of general endotracheal anesthesia, with a grade 1 view via direct laryngoscopy and extubation in the operating room. However, immediate postoperative symptoms included sore throat, left jaw, and ear pain. Despite initial normal vital signs and saturation on room air, the patient developed progressive stridor, voice hoarseness, throat pain, and rapidly enlarging left neck swelling indicative of diffuse edema on bedside ultrasound. The patient ultimately required emergency intubation after several hours despite attempts at treatment with dexamethasone, racemic epinephrine, diphenhydramine, and albuterol.

Results: Several hours after extubation, the patient decompensated, leading to respiratory failure necessitating emergency intubation in the operating room. Critical oropharyngeal and laryngeal swelling were noted during fiberoptic intubation, prompting transfer to the intensive care unit. Differential diagnoses considered during the patient’s presentation include post-extubation stridor, bronchospasm, laryngospasm, hematoma, allergic anaphylaxis, acute coronary syndrome, and angioedema from ACE inhibitor use. Workup, including CBC, BMP, troponins, CXR, and ECG, yielded normal results. CT head and neck revealed extensive, diffuse soft tissue edema in the nasopharynx, oropharynx, and left-sided mucosal spaces of the neck and larynx. Two days later, the patient was taken to the operating room with otolaryngology and found to have persistent, diffuse left-sided edema with evidence of superimposed supraglottic necrotizing soft tissue infection.

Discussion/Conclusion: Despite a lack of hemodynamic collapse or urticaria, the patient exhibited critical airway compromise due to angioedema hours after an uneventful general endotracheal anesthetic.  Non-histaminergic angioedema can result from the use of ACE inhibitors or due to hereditary C1 deficiency, although ACE inhibitor use angioedema is more likely in this patient given initiation of medication six months prior and no previous episodes of angioedema. Unlike mast cell-mediated angioedema, these types of angioedema are bradykinin-mediated and do not typically respond to antihistamines or corticosteroids. ACE inhibitor-associated angioedema can present within a week to years after the initiation of this medication. Both hereditary angioedema and ACE inhibitor angioedema can be precipitated by local tissue trauma including nontraumatic endotracheal intubation. Recognition of atypical manifestations and prompt intervention, including fiberoptic intubation, proved crucial in averting further complications.