Abstract

The present study aimed to specify diagnostics for peritonsillar abscesses (PTAs) and to clarify the role of minor salivary glands. This prospective cohort study included 112 patients with acute tonsillitis (AT) and PTA recruited at a tertiary hospital emergency department between February and October 2017. All patients completed a questionnaire concerning their current disease. Serum amylase (S-Amyl) and C-reactive protein (S-CRP) levels, tonsillar findings, and pus aspirate samples and throat cultures were analyzed. Eight of 58 PTA patients (13.8%) had no signs of tonsillar infection. The absence of tonsillar erythema and exudate was associated with low S-CRP (p<0.001) and older age (p<0.001). We also observed an inverse correlation between S-Amyl and S-CRP levels (AT, r = -0.519; PTA, r = -0.353). Therefore, we observed a group of PTA patients without signs of tonsillar infection who had significantly lower S-CRP levels than other PTA patients. These findings support that PTA may be caused by an etiology other than AT. Variations in the S-Amyl levels and a negative correlation between S-Amyl and S-CRP levels may indicate that minor salivary glands are involved in PTA development.

Highlights

  • Acute tonsillitis (AT) is a highly prevalent infection that is responsible for a large number of consultations

  • A significant inverse correlation was observed between Serum amylase (S-Amyl) and S-C-reactive protein (CRP) levels in both the acute tonsillitis (AT) and Peritonsillar abscess (PTA) groups (AT, r = -0.519, p 0.001; PTA, r = -0.353, p 0.001; Fig 1)

  • We found no differences in the S-Amyl or serum CRP (S-CRP) levels between the AT and PTA groups (S-Amyl, p = 0.767; S-CRP, p = 0.501)

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Summary

Introduction

Acute tonsillitis (AT) is a highly prevalent infection that is responsible for a large number of consultations. Peritonsillar abscess (PTA) is the most common deep head and neck infection, with an incidence of 10–41/100,000 [1,2,3,4,5], and traditionally regarded as a purulent complication of AT, but the evidence for an association between the two is uncertain. PTA may appear after tonsillectomy (TE) without tonsillar remnants, as Windfuhr et al demonstrated, and the seasonal incidence of the two entities does not follow a symmetrical pattern [1, 6,7,8]. Over the last three decades, PTA has been speculated to not necessarily arise from AT, but as a consequence of poor dental health, smoking, and salivary dysfunction. Minor salivary glands have been suggested to play a significant role in PTA [3, 8, 9].

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