Erysipelas Earwax

Erysipelas are an infectious disease that is widespread all over the world, characterized by acute serous exudative inflammation of the skin or (more rarely) of the mucous membranes, marked intoxication and contagiousness. The disease was known to Hippocrates; Galen developed his differential diagnosis, and T. Syndenham in the 17th century. First noted the similarity of erysipelas with common acute exanthems.

[1]

The causes of erysipelas

The causative agent of erysipelas is a beta-hemolytic group A streptococcus (Str. Pyogenes) or other serological types that grow in the area. For the first time these microorganisms were discovered

The outstanding German surgeon T. Bilrot in 1874. According to II Mechnikov, the greatest accumulation of microorganisms can be found in the peripheral zone of the affected skin of the erysipelas.

Erysipelas are often preceded by acute streptococcal infections in the form of angina or catarrh of the upper respiratory tract. Recurrent head or face face is usually associated with the presence of foci of chronic streptococcal infection (chronic purulent sinusitis, dental caries, periodontitis, etc.). The appearance of erysipelas is promoted by specific sensitization of the organism to streptococcus and the absence of antimicrobial immunity, as well as avitaminosis and the consumption of food, poor animal proteins.

The source of the pathogen are patients with various streptococcal infections (angina, scarlet fever, streptodermia, erysipelas, etc.). Infection of erysipelas can occur by contact through damaged skin and CO. It is also possible to air-drop the way of transmission of infection with the formation of its focus in the nasopharynx, tonsils and the subsequent drift of the microorganism to the skin by hands. Infection can also spread lymphogenous and hematogenous.

Pathogenesis of the erysipelas

Erysipelas usually begin with the tip of the nose. There arises a limited sharply hyperemic focus, which soon turns into a compact, painful, abdominal plaque, sharply delimited from the surrounding tissues, characterized by serous inflammation localized in the dermis, subcutaneous tissue, along the course of its lymphatic vessels. As a result, serous inflammation spreads to all elements of the skin and its nearest subcutaneous elements. In the future, the erysipelas darkens, and on its periphery the rapid spread of the inflammatory process begins, characterized by the fact that the zone of hyperemia and edema of the skin is sharply delimited from normal skin.

Face mug (and other areas of the body) can manifest itself in several forms, often occurring simultaneously on different sites of the skin - erythematous, erythematous-bullous, bullous-hemorrhagic, pustular, squamozoid (crustular), erythematous hemorrhagic and phlegmonous gangrenous. According to the prevalence of local manifestations, the following forms of erysipelas are distinguished: localized, widespread (wandering, creeping, migrating), metastatic with the development of distant, isolated foci of lesion. By degree of intoxication (severity of the course), the lung (grade I), moderate (II) and severe (III) forms of the disease are isolated. There is also a relapsing form characterized by long-lasting, for a number of months and years, emerging recurrent diseases.

Symptoms of erysipelas

The incubation period is from several hours to 3-5 days.

Prodroma: general malaise, mild headache, more pronounced with facial localization, slight soreness in the region of regional lymph nodes, paresthesia in the site of infection, resulting in burning and growing soreness.

The initial period and the period of the swell: an increase in body temperature to 39-40 ° C, tremendous chills, increased headache and general weakness, nausea, vomiting. In single cases in the initial period - a loose stool. Early signs of intoxication include myalgic syndrome. In places of the future erysipelas (especially in face face) - a feeling of bursting, burning; appears and intensifies the pain of regional lymph nodes and along the course of lymphatic vessels. On the skin with the erythematous form, a small reddish or pinkish spot first appears, which within a few hours turns into characteristic erythema erythema - a clearly delineated region of hyperemic skin with uneven edges; the skin is infiltrated, edematic, tense, hot to the touch, moderately painful on palpation, especially on the periphery of the erythema. In a number of cases, it is possible to detect a demarcation cushion in the form of infiltrated and elevated erythema margins. In other forms of the disease, local changes begin with the onset of erythema, against which vesicles (erythematous-bullous form), hemorrhagia (erythematous hemorrhagic form), effusion of hemorrhagic exudate and fibrin into blisters (bullous-hemorrhagic form) form. In extremely severe clinical course of the disease, necrosis of the skin and phlegmon of the underlying tissues develops in places of bullous-hemorrhagic changes (phlegmonous-necrotic form).

The period of convalescence in erythematous form usually begins on the 8th-15th day of the disease: improvement of the general condition of the patient, decrease and normalization of body temperature, disappearance of signs of intoxication; local manifestations of erysipelas undergo reverse development: the skin turns pale, the cylindrical elevations of the edges of the hyperemic areas of the skin disappear, and the epidermis peels with flaps. When the face of the scalp is hairy, hair loss, which subsequently grows again, the existing skin changes disappear completely.

In severe bullous-hemorrhagic form, the recovery period begins 3-5 weeks after the onset of the disease. In place of blisters and hemorrhages, there is usually a dark brown pigmentation of the skin. Complications in the form of phlegmon and necrosis leave behind scars and deformities of the skin.

With a frequently recurring erysipelas in the period of convalescence, there are almost always persistent residual effects in the form of infiltration, edema and skin pigmentation, and lymphostasis.

Currently, the clinical course of erysipelas is changing toward weighting. Hemorrhagic form appeared and became widespread, the number of cases with a longer fever increased, as well as the number of patients with a recurrent course, cases of comparatively slow repair in the lesion site became more frequent.

Isolated external ear infection with erysipelas usually occurs against the background of weakened immunity as a complication of purulent infection of the external auditory canal, chronic otorrhoea with purulent otitis media, damage to the integrity of the skin of the auricle and external auditory canal. In the face of the external auditory meatus, the process often extends to the tympanic membrane, causing its perforation, and passes to the tympanic cavity, provoking the inflammation of its anatomical formations. Often erysipelatous inflammation of the ear, face and scalp is complicated by otitis media, mastoiditis and sinusitis.

Diagnosis in typical cases is not difficult, and the diagnosis is based on a characteristic clinical picture. In the blood - neutrophilic leukocytosis with a shift in the leukocyte formula to the left, toxic granulocytic leukocytes, increased ESR.

Treatment of erysipelas

Hospitalization and isolation of patients. The course of treatment with antibiotics penicillin series (bicillin-5) - at least 7-10 days, even with abortive clinical course.

General treatment. Dystoxic therapy: intravenous polyionic solutions (trisol, quartrel), as well as derivatives of polyvinyl-pyrrolidone (hemodez, polidez, neohemodez, etc.).

With hemorrhagic form - ascorutia, ascorbic acid, young people - calcium gluconate. With prolonged forms with delayed skin repair - ascorbic and nicotinic acid, vitamins A, group B, multivitamin mixtures with microelements. Of nonspecific immunostimulating drugs - pentoxyl, yeast nucleic acid, methyluracil, pyrogenal, prodigiozan, preparations of celandine large.

Local treatment is indicated only with bullous-hemorrhagic form and its complications (phlegmon, necrosis). In an acute period in the presence of intact blisters, nx gently cut at the edge and after the exudate exude dressings with a 0.1% rivanol solution, 0.02% aqueous solution of furacilin. Tight bandaging is unacceptable. The duration of the dressing should not exceed 8 days. Later, with local eruptions remaining erosion, locally used, which exert a biostimulating effect, promote the regeneration of tissues ointment and gel solcoseryl, vinylin, peloidin, extericide, methyluracil ointment, etc.

After the acute inflammatory process subsides for the treatment of residual erysipelas, primarily its infiltration in the area of the former face and ER eruptions (the NSI is closed with a tight stopper of cotton wool), apply paraffin (up to 5 procedures or more).

Prophylaxis of erysipelas

Sanitation of foci of infection (purulent diseases of the ear, sinusitis, XT, pyogenic diseases of the oral cavity), observance of personal hygiene rules, prevention and timely disinfecting treatment of microtrauma, cracks, treatment of skin pustular diseases, prevention of hypothermia of the face and ears, exclusion of contact with sick erysipelas.

Patients with recurrent erysipelas and with pronounced residual events are subject to follow-up for 2 years, according to indications - with the prescription of a preventive injection of bicillin-5.

Prognosis for asterisk of auricle

In the pre-sulfonamide and preantibiotics, death, depending on the severity of the disease, was no exception. At present, it is practically excluded and depends mainly on the existing lesions of the internal organs - diseases of the cardiovascular system, kidneys, liver, pancreas (diabetes), etc.