Orolingual angioedema to alteplase. Identify, counsel and monitor at risk patients

Abstract

Orolingual angioedema (OLA) is a known complication of intravenous alteplase used to treat ischaemic stroke. The incidence may be as high as 5.1%. ACE inhibitors are thought to increase the risk of developing this potentially life-threatening complication. This case report demonstrates how we may improve in the identification of risk factors in the history; the counselling of patients appropriately; in seeking alternative therapies such as mechanical thrombectomy; and in the monitoring of patients for signs of OLA once alteplase has been given.

Institutional Incidence of Severe tPA-Induced Angioedema in Ischemic Cerebral Vascular Accidents

“…With a small population that developed severe angioedema, it is difficult to make comparisons between this group and the patients who did not develop angioedema. Lastly, to be included in this study, the patient had to have received tPA for suspected CVA as opposed to confirmed CVAs used in other studies reviewed [ 1 – 4 , 6 , 7 , 9 , 10 , 13 , 17 ]. As stated previously, cerebral ischemia increases the amount of B2 bradykinin receptors in the brain which can increase the risk of developing angioedema with tPA, but it is unclear if this increase in receptors occurs only in ischemic CVAs or in transient ischemic accidents (TIAs) as well.…”

“…Bradykinin B2 receptors are upregulated in dying neurons such as that seen in ischemic CVA [ 1 ]. 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 – 6 ].…”

“…To date, severe cases are believed to be rare with an incidence ranging from 0.18 to one percent of all patients receiving tPA, as noted in the applicable studies [ 1 – 5 , 10 , 13 , 17 ]. The remaining studies available on this topic fail to characterize the severity of angioedema which could result in an inaccurate incidence of severe tPA-induced angioedema [ 6 – 9 , 11 , 12 , 14 – 16 , 18 , 19 ]. Furthermore, there are no studies to date that evaluate the effects of length of stay and death in patients that develop severe tPA-induced angioedema.…”

Angioedema After Use of Recombinant Tissue-Type Plasminogen Activators in Stroke

“…The first argument for a pivotal role for bradykinin is the clinical observation that the type 2 bradykinin receptor antagonist icatibant and C1 inhibitor concentrate are highly effective in patients with r-tPA-induced angioedema, contrasting sharply the described effects of antihistamines, epinephrine, and steroids. [8][9][10][11][12][13][14] prestroke use of angiotensin-converting enzyme (ACE) inhibitors significantly increases the risk of developing r-tPA-induced angioedema in response to r-tPA therapy. 3,15,16 ACE degrades systemic bradykinin and SP, supported by other bradykinin metabolic enzymes such as aminopeptidase P, dipeptidyl-peptidase IV, neural endopeptidase, and carboxypeptidase N (Figure).…”