Abstract Introduction Oral angioedema is a rare but life-threatening complication of thrombolytic therapy, with an incidence of approximately 0.02 % following alteplase administration. Tenecteplase (TNK), a genetically modified tissue plasminogen activator with a longer half-life and greater fibrin specificity, has recently gained popularity as an alternative to alteplase. However, TNK-associated angioedema remains sparsely reported. We present a case of TNK-associated angioedema requiring emergent airway management. Case Presentation An 83-year-old male with a history of coronary artery disease, diastolic heart failure (LVEF 50-55%), paroxysmal atrial fibrillation on rivaroxaban, hypertension, hyperlipidemia, obstructive sleep apnea, and temporal lobe epilepsy presented with sudden speech difficulty and staring spells while gardening. CT brain revealed a small left posterior insular infarct without hemorrhage. CTA of the neck demonstrated 70-80% left internal carotid artery (ICA) stenosis and 50-70% right ICA stenosis. On arrival, his vital signs were stable, and his NIH Stroke Scale (NIHSS) score was 14. As he was within the treatment window, he received intravenous TNK for a left middle cerebral artery (MCA) stroke.Following thrombolysis, his symptoms improved dramatically (NIHSS decreased to 1 with mild expressive aphasia), and mechanical thrombectomy was deferred. Approximately 90 minutes after TNK administration, the patient developed progressive tongue and oropharyngeal swelling consistent with angioedema. He was treated with epinephrine, famotidine, and steroids and required emergent intubation for airway protection. Following intubation, he received two units of FFP and diphenhydramine, and steroids were continued for five days.He was successfully extubated on hospital day 3 after complete resolution of angioedema and remained neurologically intact. Started on dual antiplatelet therapy 24 hours post-thrombolysis and recommended Left ICA stent. Discussion Angioedema following TNK administration, though uncommon, can rapidly compromise the airway. Similar to alteplase, TNK promotes plasmin-mediated bradykinin release, leading to increased vascular permeability. The risk is higher in patients taking ACE inhibitors and those with insular cortex infarcts, due to disrupted autonomic regulation. Management includes airway protection, discontinuation of the offending agent, corticosteroids, antihistamines, and bradykinin-targeted therapies such as icatibant in refractory cases.Even though tenecteplase has pharmacological and practical advantages over alteplase, its potential to cause angioedema persists and should not be underestimated. Therefore, while TNK has been the preferred thrombolytic agent for the last several years, it is important to stay vigilant for early signs of orolingual swelling post TNK, especially in patients with predisposing risk factors. This abstract is funded by: NONE
Khan et al. (Fri,) studied this question.