4.12 Uvular edema

agk’s Library of Common Simple Emergencies

Presentation

A patient complains of a foreign body sensation or fullness in the throat, possibly associated with a muffled voice and gagging. Upon examination of the throat, the uvula is swollen, pale, and somewhat translucent (uvular hydrops). If greatly enlarged, the uvula might rest on the tongue and move in and out with respiration. There might be an associated rash or a history of exposure to phsical stimuli, allergens, or a recurrent seasonal indicence.

What to do:

• Because of the known association of uvular with hypopharyngeal edema, watch for signs of airway compromise. If a patient complains of resiratory difficulty or breathes with stridor, commence treatment with intravenous lines and intubation and cricothyrotomy equipment at the bedside, and a crosstable lateral soft tissue neck x ray to rule out epiglottic swelling.
• If there is no acute respiraory difficulty, ask about precipitating events. Consider foods, drugs, physical agents, inhalants, insect bites and hereditary angioedema.
• When fever, sore throat and pharyngeal injection are present, culture the throat with a rapid strep screen and give an antibiotic that covers Haemophilus influenzae (e.g., Biaxin, Augmentin, Bactrim).
• It is reasonable to obtain a complete blood count with a manual differential to demonstrate eosinophilia to support the possibility of an allergic reaction or a high leukocyte count with increased granulocytes and bands to support a bacterial infection.
• Initially the patient should receive parenteral H1 and H2 antihistamines like hydroxazine 50-100mg im or diphenhydramine 25-50mg iv along with cimetidine 300mg iv or po or ranitidine 50mg iv or 150mg po.
• More severe cases should receive repeated doses of epinephrine 0.3ml of 1:1000 sq every 20 minutes x3. Nebulized isomeric or racemic epinephrine or albuterol are also effective.
• Parenteral corticosteroids like SoluMedrol 125mg iv are also typically used, although efficacy remains umproven.
• If there is a history of recurrent episodes of edema and there is a family history of the same, consider ordering a C4 complement level or C’1 esterase inhibitor levels as a screening test for hereditary angioedema. In this condition, the edema often involves the uvula and soft palate together.
• Uvular decompression may be useful in patients that are resistant to medical therapy or whose symptoms progress rapidly. This procedure consists of grasping the uvula with forceps and either making several lacerations with a sterile needle or snipping the distal centimeter as a patial uvulectomy.
• All patients should be observed for an adequate period of time to insure that there is either improvement or no further worsening of the swelling before being discharged home. Upon discharge, they should receive 4-5 days of H1 and H2 blockers and steroids if required.

What not to do:

• Do not perform a comprehensive and costly laboratory evaluation on every case. do only specific tests that are clearly indicated with results that will be followed up.

Discussion

The uvula (Latin for “little grape”) is a small conical pedulous process hanging from the middle of lower border of the soft palate. It is composed of muscle, connective tissue and mucous membrane, with the bulk of the uvula consisting of glandular tissue with diffuse muscle fibers intersperced throughout. During the acts of degluttination and phonation, the uvula and soft palate are directed upward, thereby walling off the nasal cavity from the pharynx. During swallowing, this prevents ingested substances from entering the nasal cavity.

Angioedema, also known as angioneurotic edema and Quincke’s disease, is defined as a well-localized edematous condition that may variably involve the deeper skin layers and subcutaneous tissues as well as mucosal surfaces of the upper respiratory and gastrointestinal tracts.

Immediate hypersnesitivity type I reactions, seen with atopic states and specific allergen sensitivities, are the most common causes of angioedema. These reactions involve the interaction of an allergen with IgE antibodies bound to the surface of basophile or mastocytes. Physical agents, including cold, pressure, light and vibration, or processes that increase core temperature, may also cause edema throuth the IgE pathway.

Hereditary angioedema, a genetic disorder of the complement system, is characterized by either an obsence of functional deficiency of C’1 esterase inhibitor. this allows unopposed activaation of the first component of complement, with subsequent breakdown of its two substrates, the second (C’2) and fourth (C’4) components of the complement cascade. This process, in the presence of plasmin, generates a vasoactive kinin-like molecule that causes angioedema. Acquired C’1 esterase inhibitor deficiency and other complement consumption states have been described in patients with malignancies and immune complex disorders, including serum sickness and vasculidities.

Other causes of angioedema include a direct degranulation effect on mast cells and basophils by certain medications and diagnostic agents (opiates, d-tubocurarine, curare and radiocontrast materials); substances such as aspirin, nonsteroidal anti-inflammatory drugs, azo dyes and benzoates that alter the metabolism of arachidonic acid, thus increasing smooth muscle permeability; and angiotensin converting enzyme inhibitors, implicated presumably by promoting the production of bradykinin.

The known infectious causes of uvulitis include group A streptococci, Haemophilus influenzae, and Streptococcus pneumoniae. An associated cellulitis may contiguouly involve the uvula with the tonsils, posterior pharynx, or epiglottis.

References:

• Evans TC, Roberge RJ: Quincke’s disease of the uvula. Am J Emerg Med 1987;5:211-216.
• Goldberg R, Lawton R, Newton E et al: Evaluationand management of acute uvular edema. Ann Emerg Med 1993;22:251-255.

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