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.
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.
Anatomy of the oropharynx as seen through the open mouth.
Horizontal section through the mouth and oropharynx.
Note the close proximity of the peritonsillar abscess to the internal
carotid artery and the facial artery.
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.
A peritonsillar abscess. The abscess displaces the tonsil
forward and medially. The uvula is deviated towards the contralateral
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.
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