Angioedema in the emergency department: a practical guide to differential diagnosis and management

Abstract

BackgroundAngioedema is a common presentation in the emergency department (ED). Airway angioedema can be fatal; therefore, prompt diagnosis and correct treatment are vital.Objective of the reviewBased on the findings of two expert panels attended by international experts in angioedema and emergency medicine, this review aims to provide practical guidance on the diagnosis, differentiation, and management of histamine- and bradykinin-mediated angioedema in the ED.ReviewThe most common pathophysiology underlying angioedema is mediated by histamine; however, ED staff must be alert for the less common bradykinin-mediated forms of angioedema. Crucially, bradykinin-mediated angioedema does not respond to the same treatment as histamine-mediated angioedema. Bradykinin-mediated angioedema can result from many causes, including hereditary defects in C1 esterase inhibitor (C1-INH), side effects of angiotensin-converting enzyme inhibitors (ACEis), or acquired deficiency in C1-INH. The increased use of ACEis in recent decades has resulted in more frequent encounters with ACEi-induced angioedema in the ED; however, surveys have shown that many ED staff may not know how to recognize or manage bradykinin-mediated angioedema, and hospitals may not have specific medications or protocols in place.ConclusionED physicians must be aware of the different pathophysiologic pathways that lead to angioedema in order to efficiently and effectively manage these potentially fatal conditions.

The Influence of ACE Inhibition on C1-Inhibitor: A Biomarker for ACE Inhibitor-Induced Angioedema?

“…Currently, no laboratory value and no validated point-of-care diagnostic test are available to differentiate a bradykinin-mediated from a mast cell-mediated attack [30]. As we observed an interaction of ACE inhibition with C1-INH values in vitro, as well as increased C1-INH activity in patients with ACEi AE during attacks, this marker should be further evaluated.…”

Comprehensive review of cardiovascular toxicity of drugs and related agents

“…It is typically associated with ACE inhibitor therapy, where it is attributed to excessive effects induced by bradykinin, which is physiologically degraded by the ACE enzyme . Angioedema often affects soft tissue of the head such as lips, face, tongue, periorbital tissue and may cause obstruction of oropharyngeal airways that can be dangerous . Swelling is accompanied by characteristic erythema (without itching) and pain/discomfort.…”

“…The symptoms typically last for 24–72 hr, followed by spontaneous remission. The incidence of ACEi‐induced angioedema is relatively low (approximately 0.2–0.7%) with higher chance in older patients and in females as compared to males . Importantly, African Americans are four to five times more likely than Caucasians to experience angioedema.…”

“…However, sacubitril–valsartan cannot be combined with ACE inhibitors and 36 hrs washout period is necessary when switching patients from ACEi to this new treatment . Other drugs inducing nonhistamine angioedema are NSAIDs with an incidence 0.1–0.3% and the mechanisms seems to be based on COX inhibition …”

“…485,486 Angioedema often affects soft tissue of the head such as lips, face, tongue, periorbital tissue and may cause obstruction of oropharyngeal airways that can be dangerous. 487 Swelling is accompanied by characteristic erythema (without itching) and pain/discomfort. The symptoms typically last for 24-72 hr, followed by spontaneous remission.…”