Abstract
Introduction Tissue plasminogen activator (tPA) is commonly used in ischemic cerebral vascular accidents (CVAs). tPA is generally well tolerated; however, orolingual angioedema is a well-documented adverse effect. Angioedema is generally mild, transient, and unilateral but can manifest as severe, life-threatening upper airway obstruction requiring intubation. Reported incidence for all severities ranges from one to five percent, whereas reported incidence of severe cases ranges from 0.18 to 1 percent of patients receiving tPA for ischemic CVA. Angiotensin-converting enzyme (ACE) inhibitors and middle cerebral artery distribution have been associated with a higher risk of developing angioedema. The aim of this study is to evaluate the incidence of severe tPA-induced angioedema and its effects on length of stay (LOS) and death. Methods A retrospective chart review of patients receiving tPA for ischemic CVA from January 2014 through December 2016 was conducted at a large tertiary center with Comprehensive Stroke Center designation. Subjects were eighteen or older. Baseline demographics and clinical data were collected. Results 147 patients were included with four developing severe angioedema due to tPA resulting in an incidence of 2.72%. All four were female. The median LOS was thirty days for patients with angioedema and twelve days for those without. The survival probability was higher in the angioedema group and mean time to death was twenty-two days in the angioedema group and twenty-one days in the nonangioedema group. Twenty-five patients died, one from the angioedema group. ACE inhibitor use was found to have an OR of 7.72. Conclusion This study found a higher incidence of severe angioedema than that reported. Development of severe angioedema increased length of stay but was not shown to worsen outcomes in regards to death. Consistent with previous studies, ACE inhibitor use was associated with a higher risk of developing angioedema.
Highlights
Tissue plasminogen activator is commonly used in ischemic cerebral vascular accidents (CVAs). tPA is generally well tolerated; orolingual angioedema is a well-documented adverse effect
One patient developed severe angioedema five days after administration of tPA; for this patient, angioedema was thought to be due to an antibiotic and was not included in the calculation of incidence of severe tPAinduced angioedema. erefore, four patients developed severe angioedema within twenty-four hours of tPA administration and all four cases required intubation. is resulted in an incidence of 2.7% for severe tPA-induced angioedema
Odds ratios for Angiotensin-converting enzyme (ACE) inhibitor use and comorbidities for patients that developed severe angioedema are displayed in Table 2. ree of the patients were on ACE inhibitors with an odds ratio of 7.73. ree of the four patients had areas of ischemia in the middle cerebral artery territory
Summary
Tissue plasminogen activator (tPA) is commonly used in ischemic cerebral vascular accidents (CVAs). tPA is generally well tolerated; orolingual angioedema is a well-documented adverse effect. Tissue plasminogen activator (tPA) is commonly used in ischemic cerebral vascular accidents (CVAs). Angiotensin-converting enzyme (ACE) inhibitors and middle cerebral artery distribution have been associated with a higher risk of developing angioedema. 147 patients were included with four developing severe angioedema due to tPA resulting in an incidence of 2.72%. Consistent with previous studies, ACE inhibitor use was associated with a higher risk of developing angioedema. Tissue plasminogen activator (tPA) is commonly used in patients that present with acute ischemic cerebral vascular accidents (CVAs). Angiotensin-converting enzyme (ACE) inhibitors prevent bradykinin degradation allowing for accumulation of bradykinin that can cause angioedema, and it is well known that ACE inhibitor use is associated with a higher risk of developing angioedema with tPA administration [1,2,3,4,5,6]. The kinin pathway is thought to play a larger role in tPA-induced angioedema than the complement pathway
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