Angioedema from Lisinopril

Key Clinical Features

The American College of Allergy, Asthma, and Immunology recommends recognizing ACE inhibitor-induced angioedema as asymmetric, non-pitting swelling that is not pruritic and occurs without urticaria (hives) 1, 2
Treatment with ACE inhibitors has been associated with recurrent angioedema without urticaria, prominently involving the face and tongue but also other areas including rarely the bowel and extremities 2, 3
The mechanism is bradykinin-mediated (not histamine-mediated), which explains the absence of urticaria 4

Most cases of recurrent angioedema that occur with concomitant urticaria or pruritus are histamine-mediated and are best considered within the spectrum of chronic urticaria—these are NOT ACE inhibitor-induced 1, 2
If a patient presents with both angioedema and urticaria/rash while on an ACE inhibitor, this suggests an alternative diagnosis such as allergic or histamine-mediated angioedema rather than the typical ACE inhibitor class effect 5

Swelling of extremities is a possible presentation of ACE inhibitor angioedema 2, 3
Absence of skin rash, hives, or pruritus is a characteristic feature of ACE inhibitor-induced angioedema 1, 4
Symptoms can occur within the first month of therapy but may develop even after many years of continuous use 2, 3

ACE inhibitor angioedema does not reliably respond to epinephrine, antihistamines, or corticosteroids because it is bradykinin-mediated, not histamine-mediated 2, 3
The definitive management is immediate discontinuation of the ACE inhibitor 2, 4

There are published reports of deaths from ACE inhibitor-induced laryngeal edema leading to complete upper airway obstruction 2, 3
The swelling tendency can continue for at least 6 weeks after discontinuation of the ACE inhibitor 2, 3