Uvular edema, also known as Quincke's edema when it occurs as part of allergic angioedema, is the rapid swelling of the soft palatal uvula and surrounding mucosa. The uvula can enlarge two to four times its normal size, sometimes resting on the tongue and causing a globus or choking sensation. Common etiologies include IgE-mediated allergic reactions (food, drug, insect sting), bradykinin-mediated angioedema (ACE-inhibitor induced, hereditary angioedema due to C1 esterase inhibitor deficiency), local infection (uvulitis from streptococcus, Haemophilus influenzae), trauma (post-intubation, instrumentation, snoring with vibration-induced edema), and inhaled irritants (cannabis, hot vapor, chemical exposure).
Clinical presentation includes acute throat fullness, dysphagia, muffled hot-potato voice, gag reflex stimulation, and in severe cases stridor signaling impending airway obstruction. Examination reveals an enlarged, edematous, often pale or erythematous uvula. Associated findings such as lip swelling, periorbital edema, urticaria, or wheezing suggest systemic anaphylaxis, while isolated uvular swelling without urticaria points to bradykinin-mediated mechanisms. Hereditary angioedema typically presents with recurrent episodes lasting 2-5 days unresponsive to antihistamines, often with positive family history.
Management depends on etiology and severity. Allergic angioedema responds to intramuscular epinephrine (for anaphylaxis), parenteral antihistamines, and corticosteroids. ACE-inhibitor angioedema requires immediate drug discontinuation and may need icatibant (bradykinin B2 receptor antagonist) or fresh frozen plasma if severe. Hereditary angioedema is treated with C1 inhibitor concentrate, icatibant, or ecallantide. Airway protection through observation, awake fiberoptic intubation, or surgical airway is the priority in progressive swelling. Most uncomplicated cases resolve within 24-48 hours with supportive care.