Catarrhal angina

Catarrhal angina, or erythematous angina, is most often seasonal in nature and is due to the occurrence of a banal pharyngeal microbiota, which is activated as a result of a sharp seasonal change in climatic factors; in the spring - also because of the seasonal hypovitaminosis and the long absence of insolation in the winter. Great importance in the occurrence of these anginas is attached to seasonal viral infection (adenovirus), sharply reducing the local immunity of the pharynx, resulting in the activation of saprophyte microbiota. Seasonal catarrhal sinus is highly contagious and tends to spread to the mucosa of the upper and lower respiratory tract.

Pathological changes in catarrhal angina are characterized by local hyperemia and swelling of the mucous membrane of the palatine tonsils (the process is always bilateral), the formation of small local infiltrates, enhanced eavesdropping of the epithelium both on the free surface of the tonsils and in the crypt region (lacunae). As suggested by B.S. Preobrazhensky (1954), catarrhal angina occurs infrequently.

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Symptoms of catarrhal angina

Subjective symptoms occur suddenly and are manifested by headache, chills, subfebrile or up to 38 ° C body temperature, dryness in the throat and growing pain when swallowing the food lump. Children may experience seizures, secondary inflammation of the nasopharyngeal tonsils, occipital pain, and meningism. The predominance of adenovirus infection intensifies the symptoms of meningism, until the appearance of a mild Kernig symptom - the impossibility of a full extension of the leg in the knee joint after pre-bending it at right angles in the knee and hip joints. With pharyngoscopy, there is hyperemia of the mucous membrane of the pharynx, the tongue, the soft palate, a slight increase in the palatine tonsils, sometimes covered with a gentle easily removable fibrinous film, but neither ulceration nor other structural gross destructive phenomena in catarrhal angina. The inflammatory process at the onset of the disease is localized exclusively in the area of the tonsils, but can then spread to the entire lymphadenoid ring, primarily the lateral pharyngeal ridges (lymphadenoid posts) and the nasopharyngeal tonsil. Changes in blood are sometimes absent, but more often, at body temperature approaching 38-38.5 ° C, they are characteristic of a mild or moderately severe acute inflammatory process in the body.

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Catarrhal angina begins with the sudden appearance of the above subjective sensations and the initial inflammatory pharyngoscopic changes in the mucous membrane of the tonsils. To sadneniyu, dryness, perspiration in the throat after a few hours one-more often bilateral pains are associated with swallowing, painfulness upon palpation of regional lymph nodes. Pain during swallowing rapidly increases and reaches a maximum on the 2-3 day from the onset of the disease. Hyperemia and puffiness of the tonsils, very distinct in the first 2-3 days of the disease, decrease and disappear completely by the 5th day; remain only in the area of the arches for another 10-14 days.

Body temperature in the first days can be preserved at the subfebrile level (with a weak virulence of the pathogen or with a significantly reduced reactivity of the organism), but more often it reaches 38-39 ° C, and then decreases by 4-5 days from the onset of the disease up to normal values. In children, fever can last up to 7 days or more, which may indicate a complication. Pronounced and frequent attacks of chills at the onset of the disease may indicate an adverse clinical course of catarrhal angina with possible para- and metatonsillar complications. As AHMinkovsky notes (1950), the appearance of chills on the 2-3rd day of the disease is always a serious symptom, indicating the possible occurrence of septicemia and even general sepsis.

Changes in blood composition in mild form of catarrhal angina may be very slight or even at the level of the upper limit of the norm. However, when the clinical picture is expressed, they are significant: leukocytosis to (12-14) x10 ⁹ / l with a moderate neutrophilia and a shift in the leukocyte formula to the left; However, in some severe (toxic) forms of catarrhal angina, leukocytosis may be absent or even marked with leukopenia with agranulocytosis (disappearance of eosinophils, their appearance again indicates a tendency towards recovery); ESR - 10-12 mm / h. In the urine in the absence of tonsillogenic jade - traces of protein. General weakness, weakness, pain in the joints, tachycardia, tachypnea in severe forms of catarrhal sinus testify to the general toxic-allergic effect of the local inflammatory process on the body as a whole. In general, with a typical clinical course of catarrhal sinus disease in adults lasts 5-7 days with a subsequent period of incapacity for 7-10 days. In the presence of cardiac or renal complications, the patient should be examined by the appropriate specialists.

Complications of catarrhal sinus can occur both with respect to peritonsillar fiber, cellulose pharyngeal regions, for example, in the form of a pharyngeal abscess, and in the form of auricular, laryngeal and tracheobronchial formations. Complications often occur in children. They, in particular, on the soil of the sore throat may have a false cereal, manifested by stridor, spasm of the muscles of the larynx. Contributes to these complications a special structure of palatine tonsils, which is distinguished by a significant hypertrophy in the region of the lower pole extending into the region of the laryngopharynx.

The most common complication of catarrhal angina at a distance both in children and in adults is nephritis. Often after severe angina, albuminuria is observed, which can manifest itself both at the height of the disease, and for several weeks after it. In the preantibiotic and pre-sulfonamide period, cardiac and rheumatoid complications were frequent, which left incurable heart defects, joint diseases, as well as diseases of the collagen system.

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A direct diagnosis is based on an anamnesis, epidemiological data and the clinical picture described above. Catarrhal tonsillitis is differentiated from vulgar pharyngitis, which is characterized by diffuse hyperemia of the pharyngeal mucosa, especially in the back wall, where "scatter" of inflamed granules also appears. Hyperemia of the pharynx at the initial stage of the peritonsillar abscess is characterized by one-sidedness of the process and a rapidly developing clinical picture. Scarlet fever is different from catarrhal angina by several specific features. In the initial phase of scarlet fever, an enanthema is often identified, characterized by intense purple-red coloration, encompassing the mucous membrane of the tonsils, lateral ridges, soft palate and tongue. Unlike vulgar catarrhal angina, this hyperemia is not diffuse, but abruptly breaks, almost linearly, at the level of the soft palate. In contrast to the bright hyperemia of the pharynx, the tongue becomes pale, covered with a white coating, in diphtheria. As a rule, scarlet fever is accompanied by vomiting, which is not observed in catarrhal angina.

Simple catarrhal angina should also be differentiated from the syphilitic enantheme that occurs in the second stage of syphilis; the latter is characterized by total hyperemia of the mucosa and the presence of characteristic lamellar formations. From hyperemia of throat with mononucleosis, catarrhal angina differs in the absence of polyadenite. Toxic erythema of the pharynx, arising from poisoning with antipyrine, iodoform, arsenic preparations, food products, is differentiated on the basis of anamnestic data and specific features of the clinical course of these poisonings.