In this episode, I’ll discuss the treatment of ACE inhibitor induced angioedema.
Angioedema due to Angiotensin-converting enzyme (ACE) inhibitors is a rare event. Because of the high frequency of ACE inhibitor use, many patients will go on to develop ACE inhibitor induced angioedema.
Angioedema is the swelling of deep dermis, subcutaneous, or submucosal tissue due to vascular leakage. When this swelling involves the upper airway, angioedema can be life-threatening. ACE inhibitor angioedema is related to elevated levels of bradykinin.
Swelling usually develops over minutes to hours, peaks, and then resolves over 24 to 72 hours. There are no definitive tests to confirm ACE inhibitor angioedema. One unique characteristic (besides a medication history including an ACE inhibitor) that helps make the clinical diagnosis of ACE inhibitor induced angioedema is the absence of itching or urticaria.
Treatment
When you encounter a patient with ACE inhibitor induced angioedema that involves the upper airway, the first and only priority is to protect the patient’s airway.
If you hear stridor, see that the patient is drooling, using accessory muscles to breathe, or has edema of the tongue or floor of the mouth, assume that the physician will want to immediately intubate the patient and obtain the necessary medications to assist with this process. I discussed medications used during intubation in episode 15.
Because ACE inhibitor induced angioedema results from bradykinin and not histamine release, therapies that work for histamine induced angioedema are not considered effective.
If the diagnosis of ACE inhibitor induced angioedema is clear, don’t waste time with epinephrine, glucocorticoids, and antihistamines as they do not effect bradykinin or alter the course of ACE inhibitor induced angioedema.
Depending on the location of the angioedema, the physician may choose a nasal rather than oral approach to intubation.
Other treatments