Pediatric Peritonsillar Abscess Clinical Presentation
- Author: Itzhak Brook, MD, MSc; Chief Editor: Russell W Steele, MD more...
History
The following may be noted in patients with peritonsillar abscess (PTA):
- History of recurrent episodes of pharyngotonsillitis and previous peritonsillar abscess
- History of snoring or other symptoms of obstructive sleep apnea
- Sore throat/dysphagia and neck swelling and pain - Usually for 5-7 days; not improving on antibiotics
- Trismus - Pain when mouth is opened wide; secondary to irritation and reflex spasm of the internal pterygoid muscle
- Fever
- Pooling of saliva and drooling
- Tiredness, irritability, and reduced oral intake
- Muffled voice - Also called "hot potato" voice; secondary to dysfunction of the palatal muscles on the affected side, resulting in velopharyngeal insufficiency
- Referred ear pain
- Smoking - Has been found to be a risk factor in the development of peritonsillar abscess[8]
Peritonsillar abscess may have changed its characteristics in recent years; it is affecting more older patients, has a worse and longer course, and has emerged without antecedent tonsillitis or in spite of prior adequate antibiotic therapy.[9]
Physical
- Moderately uncomfortable appearing
- Febrile
- Potential respiratory distress
- Difficulty opening mouth (trismus)
- Oropharynx symptoms (See the image below for an example of an oropharynx examination.)
Examination of the oropharynx demonstrates unilateral swelling and erythema of the left tonsil with deviation of the uvula to the contralateral side. Courtesy of Michael Altieri, MD, Medifor, Inc. Used with permission. - Asymmetric swelling of the soft tissues is lateral and superior to the affected tonsil with displacement of the affected tonsil medially and anteriorly. Bilateral peritonsillar abscess is uncommon.
- Fluctuant area is palpable.
- Appearance of tonsil may be normal or may show erythema and exudates.
- Uvula is displaced to the contralateral side.
- Soft palate is red and swollen.
- Involvement is bilateral in 3% of cases.
- Halitosis
- Cervical and submandibular lymphadenopathy
- Infection: If epiglottitis or other deep neck space infection are suspected, imaging or careful examination (with the availability of an artificial airway placement) may be required.
Causes
A positive culture of aerobic and/or anaerobic pathogens is observed in 60-80% of aspirates.
Bacterial growth is often polymicrobial, including aerobic and anaerobic bacteria of oral flora origin. More than half of the aerobic (ie, Staphylococcus aureus) and anaerobic (ie, Prevotella, Porphyromonas, and Fusobacterium species) isolates can be beta-lactamase producers.
Streptococcus pyogenes may be absent in over half the cases, and the causative organisms may be anaerobic bacteria.[10]
Aerobic bacteria implicated in peritonsillar abscess include the following:
- Group A beta-hemolytic S pyogenes (most commonly isolated aerobe)
- Staphylococcus aureus (methicillin susceptible or methicillin resistant)[11]
- Alpha-hemolytic streptococci
- Coagulase-negative staphylococci
- Streptococcus pneumoniae (penicillin susceptible or penicillin resistant)
Anaerobes implicated in peritonsillar abscess include the following[2, 3] :
- Anaerobic gram-negative bacilli (eg, pigmented Prevotella and Porphyromonas species, Bacteroides species)
- Peptostreptococcus species
- Fusobacterium species (Fusobacterium nucleatum predominated in recent studies)[12]
Viruses do not seem to play a role in the pathogenesis of peritonsillar abscess.[13]
Differentiating between peritonsillar abscess and peritonsillar cellulitis is often difficult because the pathogenesis is similar and patients present with similar symptoms.[14] Only patients with a peritonsillar abscess require a drainage procedure, whereas patients with either peritonsillar abscess or peritonsillar cellulitis are treated with antibiotics.
Clinical signs such as trismus and inconsistent drooling have been associated more often with peritonsillar abscess. No method to differentiate between the two is perfect; however, current methods include the following:
- Observing the patient's response to 24-48 hours of intravenous antibiotics
- Attempting needle aspiration of the site
- Using an imaging modality such as CT scanning or ultrasonography[15, 16, 7]
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