PTA has been reported in patients who have undergone tonsillectomy.2–10
However, the majority of cases reported in the literature were found to have remnant tonsil tissue providing a potential source of infection and an associated remnant peritonsillar space walled off by scarring following surgery. Although it is appreciated that remnant tissue may be very small and not always obvious on clinical examination, eleven cases of PTA have been reported in patients without apparent residual tonsil tissue ().2–8
The additional case presented in our paper is the youngest patient reported to date and the only paediatric case.
This review suggests that patients may present with a PTA many years after a tonsillectomy has been performed and in the absence of a prior history of PTA. However, when the indication for the tonsillectomy is stated, two patients (33%) had no previous history of tonsillitis. One of these patients had a tonsillectomy performed for a recurrent PTA, suggesting an alternative source of infection preoperatively. Most patients have no infection following their tonsillectomy. A minority have a recurrent infection or suppuration in the peritonsillar tissue. The review suggests that patients respond well to conventional treatment in the form of needle aspiration or incision and drainage with antibiotics.
Peritonsillar abscess after tonsillectomy may appear to be a contradiction in terms, assuming tonsil tissue is removed and the peritonsillar space is obliterated (although in reality, it is very difficult to completely remove all tonsil tissue when performing a tonsillectomy, particularly at the lower pole and tongue base). The areolar tissue in the peritonsillar space can be divided into layers superiorly.7
If the tonsil capsule is not completely removed during the tonsillectomy, this may explain the development of a PTA in a superior location. Even if the tonsil capsule is completely removed, there may be suppuration in any remnant peritonsillar tissue. Pus may collect between the superior constrictor muscle and any fibrosis resulting from the tonsillectomy.
The aetiology of PTA formation after tonsillectomy remains uncertain but there are a number of potential explanations, assuming that there is no remnant tonsil tissue infection. Embryologically, the tonsil is derived from the second internal pharyngeal pouch. The membrane between the pouch and the cleft may rupture during development and result in an internal branchial fistula between the tonsil and the superior constrictor muscle.11
It has been claimed that a tonsillectomy may predispose patients with this congenital fistula to recurrent abscesses by resulting in scarring that obstructs drainage of an infected tract or cyst.2,5
Weber's glands are tubular mucous glands located above the capsule of the superior pole of the tonsil.12
The glands send a common duct to the tonsil and secrete saliva on to the surface of the tonsillar crypts.13
The glands may be left behind following a tonsillectomy and are therefore a potential source of suppuration after surgery.5
It has been proposed that dental disease may play a role in the aetiology of PTA formation. In a review of 84 patients (with tonsils) presenting with peritonsillitis, Fried and Forrest found that 27% gave a history of recent dental infection.14
Patients with a PTA have an increased prevalence of periodontal disease compared with patients with recurrent tonsillitis.15
There have also been reports of PTA formation following dental extraction and local anaesthetic infiltration.2
Infections of peritonsillar tissue secondary to trauma, foreign bodies, tubercular granulomas and syphilitic gummata have also been reported as potential causes of PTA formation in patients with tonsils.2
Furthermore, it has been suggested that tonsillectomy results in local immunological change that predisposes to local infection.2
Although the reported incidence of a PTA in the absence of tonsil tissue remains very low, understanding the aetiology is important. It challenges the widespread belief that PTA formation is the complication of tonsillitis and has wider implications for aiding our understanding of the complex aetiology of PTA formation in general. In particular, it might explain the source of infection in patients with a PTA without concurrent tonsillitis. The possibility of a congenital branchial fistula, Weber's glands and dental disease should be considered as potential sources of infection in all patients presenting with a PTA in the absence of tonsillitis. This may influence patient management as additional examinations and investigations may be required accordingly. Where surgical intervention is warranted, attention to an adequate tonsillectomy with excision of Weber's glands and appropriate management of branchial anomalies is important.