It is easy, especially when just starting out, to confuse an acute tonsillitis, peritonsillar phlegmon/cellulitis and a peritonsillar abscess. Below there are some general guidelines to recognizing and treating these entities.


Acute tonsillitis

The key to differentiating acute tonsillitis from peritonsillar processes is understanding that generally tonsillitis presents with symmetrically enlarged bilateral tonsils. The oropharynx may be markedly crowded however it is mainly the tonsils that are swollen – there should be good definition of the tonsil-palate interface and minimal soft palate asymmetry. The majority of patients with acute tonsillitis may be managed as outpatients and it is only severe cases (can’t take PO or airway complaints) that typically need to be admitted for observation. Treatment generally consists of a 10 day course of penicillin, augmentin (if mono has been ruled out) or clindamycin.  Patients that have poor intake secondary to pain may benefit from a short course of steroids and liquid pain medication. 

GABHS is usually the culprit for these infections.  However in patients with significant fatigue and giant 4+ tonsils, there should be high suspicion for mononucleosis. Even if the patient truly does have mono, the monospot will generally be negative for the first 2+ weeks and at least early on, a CBC looking for lymphocytosis may be helpful. 


Peritonsillar cellulitis and Peritonsillar abscess

In contrast to acute tonsillitis, patients with peritonsillar cellulitis or abscess almost uniformly present with unilateral soft palate swelling while the tonsils themselves are typically not very enlarged.  A distinguishing feature on physical examination is the inferior medial displacement of the infected tonsil with a contralateral deviation of the uvula. Patients generally appear very sick and frequently have a muffled “hot potato” voice, drooling, trismus and impressive lymphadenopathy. 

Peritonsillar cellulitis and peritonsillar abscess appear identical on examination, the only difference, obviously is that the PTA contains pus. In general it is safest to treat these 2 processes identically since it is difficult differentiate them without aspiration or I&D.  

Treatment is somewhat controversial.  All patients should be treated with a The majority of practitioners at very least recommend trial needle aspiration and if pus is aspirated, then incision and drainage may be beneficial to allow the “pus pocket” to drain.  A small minority of practitioners advocate trial antibiotics alone and only decompression if there is no response or if there is clinical decline.


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