Complications of Tonsillitis

Local (purulent) complications

The classic variant of the development of a purulent process is its spread beyond the capsule of the palatine tonsil. This leads to the formation of a peritonsillar abscess, retropharyngeal abscess, or parapharyngitis.

The most frequent pathology in this group is a peritonsillar abscess (paratonsillitis). It forms shortly after tonsillitis when inflammation spreads from the tonsillar parenchyma to the surrounding soft tissue (sometimes the source is a problematic wisdom tooth with an operculum). The disease requires emergency care.

Clinically, the abscess manifests with a sharp deterioration in condition. Patients complain of acute unilateral sore throat radiating to the ear, and the inability to swallow even saliva. Fever up to 40 °C, an earthy facial complexion, nasal voice, halitosis, and trismus—pronounced spasm of the masticatory muscles—are characteristic. On examination (pharyngoscopy), asymmetry of the soft palate, medial displacement of the tonsil, and tissue bulging are revealed.

Based on localization, four types of peritonsillar abscesses are distinguished:

• Anterosuperior;
• Anteroinferior;
• Posterior;
• Lateral — the most dangerous variant, as pus easily breaks through into the parapharyngeal space.

If the infection continues to spread through the interfascial spaces, neck phlegmon develops, and subsequently purulent tracts can reach the mediastinum, causing purulent mediastinitis. Staphylococci, streptococci, enterobacteria, and anaerobes frequently act as causative agents at this stage.

Systemic (metatonsillar) complications

Chronic inflammation in the tonsils (especially of streptococcal etiology) leads to persistent sensitization of the body. The leading position among systemic complications is occupied by tonsillocardiac syndrome — rheumatism and heart damage. Damage to the kidneys, joints, gastrointestinal tract, hematopoietic system, and the development of sepsis are also possible.

The main culprit of rheumatic fever is group A beta-hemolytic Streptococcus (GABHS), more specifically, its specific rheumatogenic M-serotypes (1, 3, 5, 6, 14, 18, 19, 24). Streptococcus possesses a powerful arsenal of pathogenicity factors:

• M-protein — the main virulence factor. It blocks the phagocytosis of the pathogen by macrophages and triggers the production of antibodies that subsequently damage the body's own tissues.
• Streptolysins O and S — destroy fibrin by activating plasmin.
• Pneumolysin — damages cell membranes.
• Hyaluronidase — breaks down connective tissue, helping bacteria move deeper.
• C5a peptidase — destroys chemotaxis factors, reducing the local immune response.

The transition of Streptococcus into L-forms ensures long-term persistence of the infection, while returning to the regular form provokes relapses of rheumatism.

Manifestations of rheumatic attack and kidney damage

If streptococcal tonsillitis triggers a rheumatic attack, inflammation can encompass practically any body system:

1. Heart: rheumatic endocarditis or myocarditis. Clinical signs of heart damage usually manifest vividly on the 5th–7th day after joint pain subsides.
2. Joints: migratory polyarthritis of large symmetrical joints. Exudation predominates in the joints, therefore, no gross scars or deformities remain after the exacerbation subsides.
3. Other organs: rheumatic pneumonia, polyserositis.

Morphologically, specific rheumatic granulomas, nonspecific exudative-proliferative infiltrates (macrophages, lymphocytes), and microcirculatory vasculitis are detected in the tissues.

A separate severe complication is acute post-streptococcal glomerulonephritis (tonsillorenal syndrome). Unlike rheumatism, it is caused by specific nephritogenic strains of GABHS. The mechanism of damage here is not associated with direct bacterial invasion: circulating immune complexes are deposited in the renal glomeruli, triggering proliferative inflammation.

Diagnosis and classification of chronic tonsillitis

The connection between complications and tonsillitis is confirmed laboratory-wise. Throat swabs culture Streptococcus group A. An increase in the titer of specific antibodies is registered in the blood: antistreptolysin O (ASO), anti-DNase B, antihyaluronidase. Simultaneous assessment of ASO and anti-DNase B possesses maximum accuracy.

The development of complications is a key criterion in establishing the diagnosis and choosing treatment tactics. B.S. Preobrazhensky's classification distinguishes simple and toxic-allergic forms (TAF):

• Simple form proceeds without systemic complications.
• Toxic-allergic form is diagnosed when conservative treatment does not work, tonsillitis is severe, or associated diseases (rheumatic carditis, nephritis) occur. Even a single case of peritonsillar abscess in the anamnesis automatically transfers tonsillitis to the TAF category.

Interestingly, complications can also develop in tonsillitis-free (non-anginal) forms, when the patient does not remember acute episodes of sore throat, but pharyngoscopy reveals adhesions, liquid pus, and foul-smelling plugs in the tonsillar crypts.

Class and exam questions

What else to study on this topic

• Morphology of the rheumatic granuloma: stages of formation and cellular composition.
• Immune complex mechanism of kidney damage in glomerulonephritis.
• Indications for surgical treatment in the toxic-allergic form of tonsillitis.
• Microflora features in the development of purulent mediastinitis and neck phlegmon.

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.