Peritonsillar Abscess

Abstract

Objective To review the literature concerning the 2 primary hypotheses put forth to explain the pathogenesis of peritonsillar abscess: “the acute tonsillitis hypothesis” (peritonsillar abscess is a complication of acute tonsillitis) and “the Weber gland hypothesis” (peritonsillar abscess is an infection of Weber’s glands). Data Sources PubMed, EMBASE. Review Methods Data supporting or negating one hypothesis or the other were elicited from the literature. Conclusions Several findings support the acute tonsillitis hypothesis. First, the 2 main pathogens in peritonsillar abscess have been recovered from pus aspirates and bilateral tonsillar tissues with high concordance rates, suggesting that both tonsils are infected in patients with peritonsillar abscess. Second, studies report signs of acute tonsillitis in the days prior to and at the time of peritonsillar abscess. Third, antibiotic treatment reduces the risk of abscess development in patients with acute tonsillitis. However, some findings suggest involvement of the Weber’s glands in peritonsillar abscess pathogenesis. First, high amylase levels have been found in peritonsillar pus. Second, the majority of peritonsillar abscesses are located at the superior tonsillar pole in proximity of the Weber’s glands. We propose a unified hypothesis whereby bacteria initially infect the tonsillar mucosa and spread via the salivary duct system to the peritonsillar space, where an abscess is formed. Implications for Practice Our findings support the rationale for antibiotic treatment of patients with severe acute tonsillitis to reduce the risk of abscess development. Improved understanding of peritonsillar abscess pathogenesis is important for the development of efficient prevention strategies.