Chronic tonsillitis - Complications

Complications arising from chronic tonsillitis are divided into local and general (peritonsillar and metatonsillar).

Local complications include:

1. paratonsillitis with periodically occurring peritonsillar abscesses;
2. exacerbation of parenchymatous tonsillitis in the form of periodically occurring sore throats;
3. regional lymphadenitis;
4. intratonsillar solitary and multiple abscesses;
5. degeneration of parenchymatous tissue into scar tissue with the loss of the palatine tonsils of their specific local and general immune functions, etc.

Common complications include:

1. acute tonsillar sepsis, the causes of which may be rough squeezing of caseous plugs from the lacunae (mechanical disruption of the tonsillar barrier) or disruption of barrier functions as a result of infectious-toxic damage to cell membranes, both from the site of infection and from the venous tonsillar plexuses and lymphatic vessels;
2. chronic sepsis, which also occurs as a result of dysfunction of the palatine tonsils under the influence of chronic infectious-allergic effects of focal infection nesting in the palatine tonsils;
3. Previous conditions can ultimately cause toxic-allergic lesions of organs and systems at a significant distance from the source of infection (septic endocarditis, rheumatism, infectious non-specific polyarthritis, nephritis, pyelitis, cholecystitis and a number of other diseases).

Among metatonsillar complications, thyroid gland damage requires special attention. As B.S. Preobrazhensky (1958) proved, there is a significant correlation between chronic tonsillitis and various types of diseases of this gland. Chronic tonsillitis is most often observed with hyperthyroidism. Disorders of other endocrine glands are also noted.

Based on the above, it should be assumed that chronic tonsillitis, starting as a local autoimmune process of an infectious-allergic nature, as the protective barriers are destroyed and a general toxic-allergic reaction develops, is transformed into a systemic pathological process in which many organs participate, which at first resist the pathological effects of pathogenic factors with the help of their internal homeostatic mechanisms, then, when these mechanisms are exhausted, they themselves become a source of infection and, thus, the vicious circle closes with the formation of the so-called pathological functional system, which begins to act according to its internal laws, as a result of which, without curative intervention from outside, the body is doomed to self-destruction.

Of the most common complications, we will focus on nephritis, rheumatism and endocarditis.

Nephritis of tonsillogenic nature is manifested by constant albuminuria and occurs with angina or peritonsillar abscess. Acute nephritis occurs in 50% of cases after angina or exacerbation of chronic tonsillitis. Focal glomerulonephritis of tonsillogenic nature occurs in 75-80% of cases. The tonsil focus maintains albuminuria and hematuria until this focus is eliminated. Exacerbation of nephritis and the appearance of arterial hypertension contribute to the exacerbation of chronic tonsillitis. It is noted that sometimes the occurrence of renal complications is facilitated by mechanical pressure on the palatine tonsils to remove caseous masses from the lacunae, the occurrence of adenoviral diseases, local and general hypothermia. Tonsillogenic renal complications should be classified as tonsillogenic nephronia, which is proven by the fact that after tonsillectomy the vicious circle is broken and the kidneys return to normal (if no irreversible changes have occurred in them).

Rheumatism. The role of chronic tonsillitis in the development of rheumatism has long been known. It has been established that in most patients the onset of the disease or its relapse is preceded by tonsillitis, pharyngitis, rhinitis or scarlet fever. G.F. Lang associated rheumatism with the allergization of the body by streptococcal infection, in particular, nesting in the palatine tonsils. According to his data, tonsillogenic rheumatism is observed in a third of cases of rheumatic infection. Usually, rheumatoid phenomena occur 3-4 weeks after a sore throat or exacerbation of chronic tonsillitis, which do not differ in any features of clinical manifestations, sometimes even without regional lymphadenitis. However, it is always possible to establish a connection between the rheumatoid reaction and the preceding tonsillogenic excess. There is reason to believe that, unlike “true” rheumatism, which is essentially one of the forms of systemic connective tissue disease, in which the process is limited only to periarticular connective tissue, in infectious arthritis, the cause of which is one or another primary source of infection, often reveals, along with lesions of the joint bags, the involvement of bone and cartilage tissue, the ligamentous articular apparatus in the pathological process, the consequence of which is the development of joint ankylosis.

Heart diseases in 90% of cases owe their origin to rheumatism. Considering the fact that the rheumatic infection itself in many cases is caused by the presence of chronic tonsillitis, it should be considered established that this disease of the palatine tonsils is directly related to the occurrence of infectious-allergic (septic) endocarditis and myocarditis. Thus, during or immediately after a sore throat or exacerbation of chronic tonsillitis, pathological signs are detected on the ECG. A close connection (reflex and humoral) of the tonsils with the heart (conducting and connective tissue) was also established experimentally. The introduction of turpentine into the palatine tonsils of experimental animals caused characteristic changes in the ECG, while such an effect on the limb did not cause such changes in the ECG.

One of the most common cardiac complications in chronic tonsillitis is the tonsillocardial syndrome, or tonsillogenic myocardial dystrophy, recognized throughout the world, caused by intoxication with substances released into the blood during chronic tonsillitis or frequent sore throats, and myocardial sensitization to these substances. Patients complain of shortness of breath and palpitations during physical exertion (less often at rest), sometimes a feeling of interruptions in the work of the heart. Objective signs of tonsillocardial syndrome are inconstant. Tachycardia is often observed, sometimes a systolic murmur is heard at the apex of the heart, caused by relative mitral insufficiency, extrasystoles. On the ECG, various conduction disturbances can be detected, not reaching a significant degree, extrasystole, changes in the T wave. Often, ECG changes are absent in the presence of unpleasant subjective sensations behind the sternum. Often, tonsillocardial syndrome acts as a precursor to tonsillogenic myocarditis, which is manifested by more pronounced disturbances in cardiac activity with signs of general inflammation (increased ESR, leukocytosis, positive test for C-reactive protein, etc.).

Based on the doctrine of focal infection, many authors in the 1930s were carried away by the theory of "portal infection", attributing to the tonsils an almost "global role" in the emergence of many diseases. They began to perform a mass removal of the palatine tonsils in various infectious and allergic diseases, as a "hotbed of infection", without having, in fact, any idea of the most important functions of this organ, especially in the early stages of postnatal ontogenesis.

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