TPA-Induced Angioedema in a Patient Taking Angiotensin Converting Enzyme Inhibitors: A Case Report and Review of the Literature

Abstract

SESSION TITLE: Nervous System Disorders in the ICU 1 SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Asymmetric Orolingual Angioedema (AOA) is a rare, but important and potentially fatal adverse drug reaction that requires prompt recognition. We present a case of AOA in a 96-year-old woman after receiving tissue plasminogen activator (tPA). AOA is characterized by often unilateral swelling of the tongue and lips that in severe cases can result in airway obstruction. In this report, we describe a patient on angiotensin converting enzyme inhibitor (ACEI) who presented with angioedema after tPA administration. CASE PRESENTATION: This is a 96 year old female with a past medical history of two transient ischemic attacks, hypertension on lisinopril, presenting with 2 hours of right sided hemiparesis and slurred speech. In the emergency room, patient’s neurologic status continued to decline to severe aphasia, right upper and lower flaccidity. NIHSS score was 20. Stroke code was activated and computed tomography of the head without contrast revealed no acute hemorrhage. tPA was administered and 11 minutes later the nurse noticed partial swelling of left side of tongue and urticaria of the right cheek. Benadryl, Epinephrine and Solu-medrol were immediately given with no interval decrease in swelling. The decision was made to intubate for airway protection. During the course of her ICU stay, patient’s swelling improved and eventual MRI was found to be negative for acute stroke. DISCUSSION: In a systematic review of manuscripts between 1950-2012, only 41 cases of tPA induced angioedema are described with an incidence ranging from 1.7 to 5.8%. While thought to be very infrequent, a trend in the increase of primary stroke centers and therefore tPA use will likely lead to an increase in adverse event reports. The pathophysiologic mechanism of this disease is poorly understood, but thought to involve plasmin and complement mediated bradykinin release. While the relationship is unclear, reports have discovered an association of AOA with middle cerebral artery infarction and prior use of ACEI. Our patient was on Lisinopril at home, but was found not to have acute infarction on MRI. As the potential of catastrophic airway compromise is high, detailed history on ACEI use, previous tPA administration, and C1-esterase inhibitor deficiency must be taken. CONCLUSIONS: In conclusion, with the development and increasingly strong evidence of benefit of early fibrinolytics in acute ischemic stroke, tPA use has increased. This is the first case of AOA at our institution. In the setting of acute stroke in patients with previous angiotensin converting inhibitor use, close monitoring is necessary post-administration in case emergent intervention is necessary. Reference #1: Hill MD, et al. Hemi-orolingual angioedema and ACE inhibition after alteplase treatment of stroke. Neurology. 2003;60(9):1525-7. Reference #2: Hill MD, et al. Anaphylactoid reactions and angioedema during alteplase treatment of acute ischemic stroke. CMAJ. 2000;162(9):1281-4. DISCLOSURE: The following authors have nothing to disclose: Christian Castaneda, Samarth Beri, Sheelan Karim No Product/Research Disclosure Information