![]() These symptoms are most prominent in ACE inhibitor-induced Angioedema. When facial swelling occurs, it will usually be swollen in the lips, tongue, and uvula. In most cases, angioedema will present with a rapid onset of swelling to the face, lips, larynx, and/or bowel. There are subtle differences in presentation among the 3 categories above. In both ACE inhibitor-induced angioedema and Hereditary Angioedema, the etiology is due to a disruption in bradykinin pathway (inhibition of bradykinin degradation from ACE inhibition, or increased production of bradykinin from C1 inhibitor deficiency). C1 inhibitor deficiency (Hereditary Angioedema)Īngioedema secondary to anaphylaxis occurs via an IgE-mediated immune response, which activates mast cells and releases numerous inflammatory compounds, increasing vascular permeability and causing the resultant angioedema.Angiotensin Converting Enzyme (ACE) inhibitor-induced Angioedema.While there are numerous causes and etiologies of facial angioedema, for emergency physicians, three important causes of angioedema to consider are: This will usually present rapidly, with initial onset within minutes. Angioedema is defined as subcutaneous swelling resulting from fluid extravasation into interstitial tissue. Immediate life-threatening causes of Facial Swelling AngioedemaĪngioedema is one of the most important “can’t miss” cause of facial swelling. The bolded differentials are considered “can’t miss” diagnoses to always consider given immediate life threat. ![]() ![]() While the causes are expansive in nature, here are some of the important ones to consider. We can separate the differential of facial swelling into categories based on the location of the swelling. As emergency clinicians, it is important to distinguish the life-threatening causes of facial swelling from the less emergent causes. The etiologies of facial swelling can vary from a dental infection, to a decompensated Ludwig’s angina that is compromising the airway. Backgroundįacial Swelling is a complaint with a wide differential. She did bring a list of her medications, and of note, was recently started on Lisinopril for her HTN. She tries to tell you more history, but given her significant swelling and respiratory distress, you are unable to understand her. Your nurses quickly hook the patient up to the monitor, and she is noted to have an oxygen saturation in the 80’s. As you go to see her, you see a woman in distress: she has significant angioedema of the tongue/lips, tripoding, tachypneic, drooling with stridorous respirations. Your new patient is a 60-year-old female, with history of HTN, who presents with facial swelling. Suddenly, a tech quickly brings a new patient in a wheelchair. It’s a relatively slow day during the beginning of your shift in the critical care pod. Author: Winford Ko, MD (Emergency Medicine Resident, UT Southwestern/Parkland Memorial Hospital, Dallas, TX) // Edited by: Alex Koyfman, MD and Brit Long, MD Case
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