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Emergency Department visits for peritonsillar abscesses are quite frequent. One recent study cited an incidence of approximately 45,000 cases of this disease process per year.1 The mean age of affected patients is 25 years. It is a relatively rare finding before the age of 5 years. There remains a fair amount of controversy in the literature regarding the optimal antibiotic choice and the mechanism of drainage. The objective for the Emergency Physician remains to make an accurate diagnosis, to institute appropriate care, and to arrange adequate follow-up.

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The anatomy of the oral cavity is relatively simple (Figure 151-1). The peritonsillar abscess can be found posterolateral to the palatine tonsil and posterior to the palatoglossal fold (or arch). Note the close proximity of the internal carotid artery and the facial artery to the peritonsillar abscess (Figure 151-2). Use extreme care to not penetrate too deeply and lacerate these arteries.

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Figure 151-1
Graphic Jump Location

Anatomy of the oropharynx as seen through the open mouth.

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Figure 151-2
Graphic Jump Location

Horizontal section through the mouth and oropharynx. Note the close proximity of the peritonsillar abscess to the internal carotid artery and the facial artery.

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Most patients will have had symptoms for approximately 4 days by the time abscess formation has occurred. The most common symptoms include fever, sore throat, dysphagia, and trismus. Physical examination will reveal a nonexudative pharyngitis in the majority of cases, soft palate edema, a bulging prominent tonsil, and uveal deviation away from the abscessed tonsil (Figure 151-3). The differential diagnosis includes infectious mononucleosis, leukemias, odontogenic infections, and aneurysms of the internal carotid artery.

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Figure 151-3
Graphic Jump Location

A peritonsillar abscess. The abscess displaces the tonsil forward and medially. The uvula is deviated towards the contralateral side.

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The peritonsillar abscess has been attributed to progression and direct extension of an acute exudative pharyngitis. More recent work has described a group of salivary glands, Weber’s glands, located in the supratonsillar space as the actual site of bacterial invasion and subsequent abscess formation.2 The bacterial inoculum results in tissue necrosis and pus formation typically located between the tonsillar capsule and the lateral pharyngeal wall and/or the supratonsillar space. Progression of pus formation and cellulitis within the supratonsillar space results in a gradual involvement of the surrounding musculature, particularly the internal pterygoids, leading to spasm and the classic trismus seen with this disease.

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The most common isolate found on culture remains group A beta-hemolytic streptococci.3 The abscess is often polymicrobial and includes group A beta-hemolytic streptococci, Staphylococcus aureus, Bacteroides fragilis, and Bacteroides melaninogenicus. There is an increasing prevalence of beta-lactamase producing organisms.3

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