ED Management of Patients With ACE-Inhibitor Angioedema
ED Management of Patients With ACE-Inhibitor Angioedema
Background: Angiotensin-converting-enzyme inhibitors (ACEI) are one of the most prescribed medications worldwide. Angioedema is a well-recognized adverse effect of this class of medications, with a reported incidence of ACEI angioedema of up to 1.0%. Of importance to note, ACEI angioedema is a class effect and is not dose dependent. The primary goal of this literature search was to determine the appropriate Emergency Department management of patients with ACEI angioedema.
Methods: A MEDLINE literature search from January 1990 to August 2012 and limited to human studies written in English for articles with keywords of ACEI angioedema. Guideline statements and non-systematic reviews were excluded. Studies identified then underwent a structured review from which results could be evaluated.
Results: Five hundred sixty-two papers on ACEI angioedema were screened and 27 appropriate articles were rigorously reviewed in detail and recommendations given.
Conclusion: The literature search did not support any specific treatment protocol with a high level of evidence due to the limited—and limitations of the—available studies.
Angiotensin-converting enzyme (ACE) inhibitors have become one of the most prescribed medications worldwide. Angioedema is a well-recognized adverse effect of this class of medications, with a reported incidence of ACE inhibitor (ACEI) angioedema ranging from 0.1% to 1.0%. ACEI angioedema is a class effect and is not dose dependent, and thus, symptoms can occur any time from a few hours up to 10 years after the initial dose. In fact, up to 40% of patients with ACEI angioedema present months to years after their initial dose.
The pathophysiology of ACEI angioedema remains controversial. Decreased degradation of bradykinin, a potent vasodilator that increases vascular permeability, is thought to be the primary pathophysiologic process for ACEI-induced angioedema. C1-inhibitor abnormalities, carboxyalkyl dipeptide N, urinary kallikrein, and inflammatory mediators such as interleukin-1 and tumor necrosis factor have also been proposed as mediators for ACEI angioedema.
This article seeks to review the medical literature on the topic of treatment for ACEI angioedema and to offer evidence-based recommendations to emergency physicians for evaluation and treatment of patients who present with this diagnosis. This work was done at the request of, and published as a clinical practice statement by, the American Academy of Emergency Medicine Clinical Guidelines Committee.
Abstract and Introduction
Abstract
Background: Angiotensin-converting-enzyme inhibitors (ACEI) are one of the most prescribed medications worldwide. Angioedema is a well-recognized adverse effect of this class of medications, with a reported incidence of ACEI angioedema of up to 1.0%. Of importance to note, ACEI angioedema is a class effect and is not dose dependent. The primary goal of this literature search was to determine the appropriate Emergency Department management of patients with ACEI angioedema.
Methods: A MEDLINE literature search from January 1990 to August 2012 and limited to human studies written in English for articles with keywords of ACEI angioedema. Guideline statements and non-systematic reviews were excluded. Studies identified then underwent a structured review from which results could be evaluated.
Results: Five hundred sixty-two papers on ACEI angioedema were screened and 27 appropriate articles were rigorously reviewed in detail and recommendations given.
Conclusion: The literature search did not support any specific treatment protocol with a high level of evidence due to the limited—and limitations of the—available studies.
Introduction
Angiotensin-converting enzyme (ACE) inhibitors have become one of the most prescribed medications worldwide. Angioedema is a well-recognized adverse effect of this class of medications, with a reported incidence of ACE inhibitor (ACEI) angioedema ranging from 0.1% to 1.0%. ACEI angioedema is a class effect and is not dose dependent, and thus, symptoms can occur any time from a few hours up to 10 years after the initial dose. In fact, up to 40% of patients with ACEI angioedema present months to years after their initial dose.
The pathophysiology of ACEI angioedema remains controversial. Decreased degradation of bradykinin, a potent vasodilator that increases vascular permeability, is thought to be the primary pathophysiologic process for ACEI-induced angioedema. C1-inhibitor abnormalities, carboxyalkyl dipeptide N, urinary kallikrein, and inflammatory mediators such as interleukin-1 and tumor necrosis factor have also been proposed as mediators for ACEI angioedema.
This article seeks to review the medical literature on the topic of treatment for ACEI angioedema and to offer evidence-based recommendations to emergency physicians for evaluation and treatment of patients who present with this diagnosis. This work was done at the request of, and published as a clinical practice statement by, the American Academy of Emergency Medicine Clinical Guidelines Committee.
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