ACE inhibitor-induced angioedema
ACE inhibitor-induced angioedema is bradykinin-mediated swelling, typically of the face, lips, and tongue, caused by impaired bradykinin degradation during ACE inhibitor therapy. It occurs without urticaria, can begin months to years after starting the drug, and does not respond to epinephrine, antihistamines, or steroids, so management is airway protection and permanent discontinuation of the class.
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What this article covers
- Overview
Definition: ACE inhibitor-induced angioedema is bradykinin-mediated, non-pitting swelling of the deep tissues, most often the face, lips, and tongue, arising during angiotensin-converting enzyme (ACE) inhibitor therapy.
- Epidemiology
Most common bradykinin angioedema in practice: ACE inhibitors are the leading drug cause of angioedema seen in emergency care.
- Risk factors
ACE inhibitor therapy: the necessary exposure, with risk across the whole class.
- Pathophysiology
ACE normally degrades bradykinin: angiotensin-converting enzyme inactivates bradykinin, so inhibiting ACE allows bradykinin to accumulate.
- Clinical features
Non-pitting facial swelling: lips, tongue, and periorbital tissue, developing over hours.
- Differential diagnosis
Allergic (histaminergic) angioedema: urticaria and pruritus present and responsive to epinephrine and antihistamines, unlike the urticaria-free, treatment-resistant swelling of ACE inhibitor angioedema (Angioedema).
- Diagnosis
Diagnose clinically by the combination of features: bradykinin-mediated angioedema is confirmed as ACE inhibitor-induced when a patient on an ACE inhibitor develops non-pitting angioedema without…
- Management
First, secure the airway (the initial step): assess tongue, floor-of-mouth, and laryngeal involvement, and intubate early (or perform a surgical airway) for progressive swelling, stridor, or voice change, because deterioration can be sudden.
- Complications
Airway obstruction and asphyxiation: the principal danger, from tongue and laryngeal swelling.
- Prognosis
Excellent once the drug is stopped: swelling resolves over 1 to 3 days and does not recur if the class is avoided.
- Prevention
Permanently avoid all ACE inhibitors after an episode and record a class allergy.
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Related articles
- Angioedema
Angioedema is self-limited, non-pitting swelling of the deep dermis and submucosa that follows one of two mechanisms: mast cell (histamine) mediated, which occurs with urticaria and responds to epinephrine and antihistamines, or bradykinin mediated, which occurs without urticaria and does not. Distinguishing the two determines whether treatment is allergic therapy or bradykinin-targeted therapy, and airway involvement is the central danger.
- Hereditary angioedema
Hereditary angioedema is an autosomal dominant deficiency of C1 inhibitor that lets kallikrein generate excess bradykinin, causing recurrent bradykinin-mediated angioedema without urticaria. Attacks do not respond to epinephrine, antihistamines, or steroids, and a low C4 is the screening clue; treatment is airway protection with bradykinin-targeted on-demand therapy and long-term prophylaxis.
- Anaphylaxis
Anaphylaxis is an acute, potentially fatal systemic hypersensitivity reaction from massive mast cell and basophil mediator release, presenting within minutes as skin, respiratory, cardiovascular, and gastrointestinal involvement after allergen exposure. It is a clinical, treat-first diagnosis, and intramuscular epinephrine is the immediate life-saving therapy.