Alteplase associated Orolingual angioedema: A case report and literature review

Abstract

Objective: Orolingual angioedema (OA) is a rare but life-threatening complication of intravenous thrombolysis using alteplase. Angioedema can be caused by almost any medication. Administration of recombinant tissue plasminogen activator causes atypical angioedema. This study aimed to investigate factors related to and treatment of OA after thrombolysis with alteplase. Case report: We describe the case of a 53-year-old man with a history of hypertension managed with enalapril, who presented with ischemic cerebrovascular stroke. Intravenous alteplase was administered, and within 54 minutes, the patient developed severe orolingual edema requiring emergent intubation. Subsequent imaging revealed an acute-to-subacute infarct in the left occipital lobe of the posterior cerebral artery. Results: The most common factor for increased risk of OA after recombinant tissue plasminogen activator was concomitant use of angiotensin-converting enzyme inhibitors (ACEI). Conclusion: Before intravenous thrombolytic therapy, patients should be asked if they have a history of allergies, are currently using ACEI, and try to avoid using ACEI antihypertensive drugs before and after thrombolytic therapy.

Bradykinin Metabolism and Drug-Induced Angioedema

“…The recombinant serine proteases cleave plasminogen to plasmin, and in addition to their thrombolytic effects, activate the kinin pathway by converting Factor XII to Factor XIIa, with increased production of BK and AE usually appearing a few hours after thrombolytic treatment. AE is asymmetric in many cases, and mainly contralateral to the ischemic hemisphere, suggesting that infarction of the insular cortex could lead to contralateral autonomic dysfunction [101][102][103]. In addition, cerebral damage secondary to brain ischemia can lead to BK release [104].…”

“…usually appearing a few hours after thrombolytic treatment. AE is asymmetric in many cases, and mainly contralateral to the ischemic hemisphere, suggesting that infarction of the insular cortex could lead to contralateral autonomic dysfunction [101][102][103]. In addition, cerebral damage secondary to brain ischemia can lead to BK release [104].…”