Catarrhal sore throat

Catarrhal tonsillitis, or erythematous tonsillitis, is most often seasonal in nature and owes its occurrence to the banal pharyngeal microbiota, which is activated as a result of a sharp seasonal change in climatic factors; in the spring - also due to interseasonal hypovitaminosis and a long absence of insolation in the winter. Great importance in the occurrence of these tonsillitis is given to seasonal viral infection (adenoviruses), which sharply reduces the local immunity of the pharynx, as a result of which the saprophytic microbiota is activated. Seasonal catarrhal tonsillitis is characterized by significant contagiousness and has a tendency to spread to the mucous membrane of the upper and lower respiratory tract.

Pathological changes in catarrhal tonsillitis are characterized by local hyperemia and edema of the mucous membrane of the palatine tonsils (the process is always bilateral), the formation of small local infiltrates, increased auscultation of the epithelium both on the free surface of the tonsils and in the area of the crypts (lacunae). According to B.S. Preobrazhensky (1954), catarrhal tonsillitis is rare.

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Symptoms of catarrhal tonsillitis

Subjective symptoms appear suddenly and are manifested by headache, chills, subfebrile or up to 38°C body temperature, dry throat and increasing pain when swallowing a bolus. Children may experience convulsions, secondary inflammation of the nasopharyngeal tonsil, occipital pain, and meningism. The prevalence of adenovirus infection increases the symptoms of meningism, up to the appearance of a mild Kernig's symptom - the inability to fully extend the leg at the knee joint after preliminary bending it at a right angle at the knee and hip joints. Pharyngoscopy reveals hyperemia of the mucous membrane of the pharynx, uvula, soft palate, a slight increase in the palatine tonsils, sometimes covered with a delicate, easily removed fibrinous film, but no ulcers or other structural gross destructive phenomena are observed in catarrhal angina. The inflammatory process at the beginning of the disease is localized exclusively in the palatine tonsils, but can then spread to the entire lymphadenoid ring, primarily to the lateral pharyngeal ridges (lymphadenoid columns) and the nasopharyngeal tonsil. Changes in the blood are sometimes absent, but more often, at a body temperature approaching 38-38.5 ° C, they are characteristic of a mild or moderate acute inflammatory process in the body.

How does catarrhal tonsillitis progress?

Catarrhal tonsillitis begins with the sudden appearance of the above subjective sensations and initial inflammatory pharyngoscopic changes in the mucous membrane of the tonsils. Soreness, dryness, and irritation in the throat are joined after a few hours by one-sided, more often bilateral, pain when swallowing, and tenderness when palpating the regional lymph nodes. Pain when swallowing quickly increases and reaches a maximum on the 2nd-3rd day from the onset of the disease. Hyperemia and swelling of the tonsils, very distinct in the first 2-3 days of the disease, decrease and completely disappear by the 5th day; they persist only in the area of the arches for another 10-14 days.

The body temperature in the first days may remain at a subfebrile level (with weak virulence of the pathogen or with significantly reduced reactivity of the body), but most often it reaches 38-39 ° C, and then within 4-5 days from the onset of the disease it begins to decrease, dropping to normal values. In children, an increase in body temperature can last up to 7 days or more, which may indicate a complication. Severe and frequent attacks of chills at the onset of the disease may indicate an unfavorable clinical course of catarrhal tonsillitis with possible para- and metatonsillar complications. As noted by A.Kh. Minkovsky (1950), the appearance of chills on the 2nd-3rd day of the disease is always a serious symptom indicating the possible occurrence of septicemia and even general sepsis.

Changes in the blood composition in mild catarrhal tonsillitis may be very insignificant or even at the upper limit of normal. However, in severe clinical presentations, they are significant: leukocytosis up to (12-14) x 10 ⁹ /l with moderate neutrophilia and a shift in the leukocyte formula to the left; however, in some severe (toxic) forms of catarrhal tonsillitis, leukocytosis may be absent or even leukopenia with signs of agranulocytosis may be observed (disappearance of eosinophils; their reappearance indicates a tendency to recovery); ESR - 10-12 mm / h. In the urine, in the absence of tonsillogenic nephritis - traces of protein. General fatigue, weakness, joint pain, tachycardia, tachypnea in severe forms of catarrhal tonsillitis indicate a general toxic-allergic effect of the local inflammatory process on the body as a whole. In general, with a typical clinical course of catarrhal angina, the disease in adults lasts 5-7 days, followed by a period of incapacity for work for 7-10 days. In the presence of cardiac or renal complications, the patient is subject to examination by appropriate specialists.

Complications in catarrhal tonsillitis may arise both in relation to the peritonsillar tissue, the tissue of the pharyngeal regions, for example in the form of a retropharyngeal abscess, and in the form of auricular, laryngeal and tracheobronchial formations. Complications more often occur in children. In particular, false croup may occur in them due to tonsillitis, manifested by stridor, spasm of the muscles of the larynx. These complications are facilitated by the special structure of the palatine tonsils, characterized by significant hypertrophy in the area of the lower pole, extending to the area of the laryngopharynx.

The most common complication of catarrhal tonsillitis at a distance in both children and adults is nephritis. Albuminuria is often observed after severe tonsillitis, which can manifest itself both at the height of the disease and for several weeks after it. In the pre-antibiotic and pre-sulfanilamide period, cardiac and rheumatoid complications were common, which left behind incurable heart defects, joint diseases, and diseases of the collagen system.

How is catarrhal tonsillitis recognized?

Direct diagnosis is based on anamnesis, epidemiological data and the clinical picture described above. Catarrhal angina is differentiated from vulgar pharyngitis, which is characterized by diffuse hyperemia of the mucous membrane of the pharynx, especially its posterior wall, where a "scattering" of inflamed granules is also detected. Hyperemia of the pharynx at the initial stage of peritonsillar abscess is characterized by a one-sided process and a rapidly developing clinical picture. Scarlet fever angina differs from catarrhal angina by several specific signs. In the initial phase of scarlet fever, enanthem is often determined, characterized by an intense purple-red color, covering the mucous membrane of the tonsils, lateral ridges, soft palate and uvula. Unlike vulgar catarrhal angina, this hyperemia is not diffuse, but abruptly breaks off, almost linearly, at the level of the soft palate. In contrast to the bright hyperemia of the pharynx, the tongue in diphtheria appears pale, covered with a white coating. As a rule, scarlet fever tonsillitis is accompanied by vomiting attacks, which is not observed in catarrhal tonsillitis.

Simple catarrhal angina should also be differentiated from syphilitic enanthema, which occurs in the second stage of syphilis; the latter is characterized by total hyperemia of the mucous membrane and the presence of characteristic lamellar formations. Catarrhal angina differs from hyperemia of the pharynx in mononucleosis by the absence of polyadenitis. Toxic erythema of the pharynx, which occurs in poisoning with antipyrine, iodoform, arsenic preparations, and food products, is differentiated based on anamnestic data and specific features of the clinical course of these poisonings.