Chronic tonsillitis: complications

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

Local complications include:

1. paratonzillit with periodically arising peritonsillar abscesses;
2. exacerbation of parenchymal tonsillitis in the form of recurring angina;
3. regional lymphadenitis;
4. intratonsillar solitary and multiple abscesses;
5. the degeneration of the parenchymal tissue into the cicatricial with the loss of palatine tonsils of its specific local and general immune functions, etc.

Common complications include:

1. acute tonsillar sepsis, the causes of which can be coarse squeezing out of the lacunae of caseous plugs (mechanical violation of GHB) or violation of barrier functions as a result of infectious-toxic damage to cell membranes, both from the site of infection, and from venous amygdala plexuses and lymphatic vessels;
2. chroniosepsis, which also occurs as a result of impaired GHB function under the influence of chronic infectious and allergic effects of focal infection nesting in the palatine tonsils;
3. the previous conditions can ultimately lead to toxic-allergic lesions of organs and systems at a considerable distance from the source of infection (septic endocarditis, rheumatism, infectious nonspecific polyarthritis, nephritis, pyelitis, cholecystitis and a number of other diseases).

Among metatonsillar complications, special attention should be paid to thyroid damage. As B.S. Preobrazhensky proved (1958), there is a significant correlation between chronic tonsillitis and various types of diseases of this gland. Most often, chronic tonsillitis is observed in hyperthyroidism. There are also violations of other endocrine glands.

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

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

Jade of tonsillogenic nature is manifested by permanent 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 tonzillogenic nature occurs in 75-80% of cases. The almond focus supports albuminuria and hematuria until this hearth is eradicated. Exacerbation of jade and the appearance of arterial gingertenzii contribute to 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 lacunae, the appearance of adenoviral diseases, local and general hypothermia. Tonziglonal renal compliments should be attributed to tonzillogenic nephron- ism, which is proved by the fact that after a tonzillectomy the vicious circle is broken and the kidneys come to a state of norm (unless irreversible changes occurred in them).

Rheumatism. The role of chronic tonsillitis in the occurrence of rheumatism is known for a long time. It was found that in most patients the onset of the disease or its recurrence is preceded by angina, pharyngitis, rhinitis or scarlet fever. GF Lang linked rheumatism with allergic organism of streptococcal infection, in particular, nesting in palatine tonsils. According to him, tonsillogenic rheumatism is observed in a third of cases of rheumatic infection. Usually rheumatoid phenomena occur 3-4 weeks after the disease with angina or exacerbation of chronic tonsillitis, not differing 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, in contrast to "true" rheumatism, which is in fact one of the forms of a systemic connective tissue disease, in which the process is confined only to the periarticular connective tissue, infectious arthritis, caused by one or another primary infection site, is often is found, along with lesions of articular bags, involvement in the pathological process of bone and cartilaginous tissue, ligamentous articular apparatus, the consequence of which is the development of joint ankylosis.

Heart disease in 90% of cases due to its origin rheumatism. Given the fact that the rheumatic infection itself is in many cases caused by the presence of chronic tonsillitis, it should be considered established that this disease of the tonsils is directly related to the emergence of infectious-allergic (septic) endocarditis and myocarditis. So, during or immediately after the transferred angina or exacerbation of chronic tonsillitis, pathological signs on the ECG are revealed. A close connection (reflex and humoral) of the tonsils with the heart (conducting and connective tissue) was established and experimentally. The introduction of turpentine into the palatine tonsils to the experimental animals caused characteristic changes in the ECG, while such an effect on the finiteness of such ECG changes did not cause.

One of the most frequent cardiac complications in chronic tonsillitis is the worldwide recognized tonzillocardial syndrome, or tonsillogenic myocardial dystrophy, which occurs by intoxication with substances released into the blood in chronic tonsillitis or frequent tonsillitis, and sensitization of the myocardium to these substances. Patients complain of shortness of breath and heartbeat with physical exertion (less often at rest), sometimes a feeling of disruption in the work of the heart. Objective signs of tonsillocardial syndrome are fickle. Often observed tachycardia, sometimes a systolic murmur on the apex of the heart, caused by relative mitral insufficiency, extrasystoles is heard. On the ECG, you can identify various conduction abnormalities that do not reach 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 of tonsillogenic myocarditis, manifested by more severe cardiac disturbances 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 30s of the last century were carried away by the theory of "portal infection", attributing the tonsils almost a "global role" in the occurrence of a variety of diseases. They began to produce general removal of palatine tonsils with various infectious allergic diseases, as a "hotbed of infection", without, in fact, any notions about the most important functions of this organ, especially in the early stages of postnatal ontogenesis.

[1], [2], [3], [4], [5], [6], [7]