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Lecture notes, cheat sheets
Dermatovenerology. Eczema (most important)
Directory / Lecture notes, cheat sheets Table of contents (expand) LECTURE No. 13. Eczema Eczema is understood as a chronic persistently relapsing skin disease, manifested by a characteristic eczematous inflammatory reaction of the skin (in the form of grouped small vesicles) caused by various exogenous and endogenous factors that lead to the development of polyvalent skin sensitivity in patients. In true eczema, skin allergy tests fail to identify the specific allergen that directly caused the inflammatory response. Eczematous lesions appear at the sites of application of several standard allergens. Etiology and pathogenesis. Eczema is a disease of the whole body with characteristic manifestations on the skin. The same clinical forms of eczema (nummular, dyshidrotic eczema, eczematide) may have different etiologies and pathogenesis, on the basis of which the classification of eczema has been developed. 1. Predominantly exogenous eczema: 1) eczema of the hands and feet; 2) dyshidrotic; 3) professional. 2. Predominantly endogenous eczema: 1) eczema of the hands and feet; 2) dyshidrotic; 3) nummular (plaque); 4) eczematid (abortive plaque). 3. Microbial eczema: 1) nummular (plaque); 2) eczematid (abortive plaque); 3) paratraumatic; 4) varicose; 5) mycotic; 6) intertriginous. Predominantly exogenous eczema can be of allergic and non-allergic origin. In allergic genesis, an allergic reaction is a manifestation of delayed-type hypersensitivity in response to repeated exposure to allergens with suppression of cellular and humoral immunity. Often, exogenous eczema develops as a result of allergic contact dermatitis with its frequent relapses and the formation of polyvalent sensitization and autosensitization in the patient. With reduced skin tolerance to irritants, a non-allergic inflammatory eczematous reaction occurs in places of constantly repeated exposure to subtoxic agents (alkalis, detergents, organic solvents, some mineral oils, as well as water, humid and cold air, mechanical irritation). In endogenous (atopic) eczema, constitutional (endogenous) influences prevail, which are genetically predetermined and regulate the functions of the immune, hormonal, neurovegetative systems, as well as the structural and functional properties of the skin. There are violations of cellular and humoral immunity. In an extensive third group - microbial eczema - its various clinical forms are combined. In this group, the occurrence of an eczematous reaction is equally influenced by both an exogenous factor (microbial flora) and an endogenous factor - an acquired temporary local disorder in the regulation of skin functions. Long-acting chronic dystrophic disorders in the skin or subtoxic effects as a result of cumulation lead to local disturbances in its function and structure. Clinic. Eczema can begin acutely or chronically and then usually lasts a long time with a tendency to relapse. Any area of the skin can be affected, but more often eczema occurs in open areas accessible to various environmental influences (on the hands, face, feet, legs). Regardless of the location, the morphological manifestations of the disease remain the same. The only exception is eczema of the palms and soles, where due to the thickness of the stratum corneum of the epidermis, eczema manifests itself not as microvesicles, but as large multi-chamber blisters. In the acute phase, eczema is manifested by a rash on hyperemic and slightly swollen skin of small, closely grouped papules that quickly transform into tiny vesicles (the so-called microvesicles), which are located in groups and do not merge with each other. Quickly opening, the bubbles form small point erosions that separate the serous exudate. As the process subsides, small-drop wetting decreases, some of the vesicles, without opening, dry up with the formation of serous crusts, a small, bran-like peeling appears (subacute phase). Since eczema develops in jerks, all of the listed primary elements of the rash (erythema, ephemeral micropapules, microvesicles) and secondary ones (erosion with small droplets of weeping, serous crusts, pityriasis scales) are usually present in the lesion at the same time. All this determines the polymorphism of rashes characteristic of eczema: true and false (evolutionary). As the process progresses, the lesions, which have different sizes and usually blurred outlines, increase due to peripheral growth. Rashes appear in symmetrical areas and in the distance. Morphologically, secondary rashes are most often represented by erythematosquamous or papulovesicular elements, although macular, small-papular and bullous rashes are also possible. These rashes usually regress without a trace 2-3 weeks after the acute manifestations in the main focus have subsided. In some cases, eczema can reach significant spread. Subjectively, patients in the acute stage of eczema are bothered by a burning sensation and itching of the skin, and when acute inflammatory phenomena subside, they are bothered by painful itching. The predominance of small yellowish crusts and bran-like scales in clinical manifestations characterizes the regression of the disease. In the future, complete resolution of rashes or transition to the chronic stage of the disease is possible. In this case, infiltration, peeling and thickening of the affected area of the skin increase, the skin pattern (lichenification) intensifies. The color of the skin takes on a stagnant color with a brownish tinge. With an exacerbation in the focus, small vesicles, punctate erosions and crusts appear again against the background of active hyperemia. The course of eczema is characterized by duration, a tendency to chronicity and frequent relapses. Exacerbation can not always be associated with the irritating effect of contact allergens. The influence of neuroreflex, immune and endocrine disorders is more clearly revealed. The course of eczema is influenced by psycho-emotional overload, immune and endocrine dysfunctions, foci of chronic infection and some other concomitant diseases. The emerging state of increased skin sensitivity to exogenous stimuli, manifested by polyvalent sensitization, does not remain constant all the time. It gradually changes depending on the severity of compensatory and adaptive mechanisms. This leads to the undulating course of the disease characteristic of eczema. Hand eczema occurs in patients with a history of atopic dermatitis. The dyshidrotic form of eczema is formed on the palms and soles more often in individuals with a pronounced imbalance of the autonomic nervous system (with increased sweating, persistent red dermographism, vascular lability) and with atopy. Exacerbations are more often observed in the winter season, although some relapses occur in hot weather. Dyshidrotic eczema may occur initially, but patients often have a history of allergic dermatitis. The skin of the palms and soles is affected, however, in some cases, a gradual transition of rashes to the lateral surfaces of the fingers and the back surface of the hands and feet is possible. The clinical feature of this form of eczema is large, pea-sized, dense multi-chamber blisters, which is due to the thick stratum corneum. Therefore, there is no hyperemia and swelling. Bubbles persist for a long time without opening. The lesion gradually spreads to the interdigital spaces and the rear of the hands and feet. In this localization hyperemia and puffiness are already expressed, there are small superficial rapidly opening vesicles and erosions with a characteristic small droplet weeping. If a pyogenic infection joins, the contents of the cavity elements become purulent, regional lymphangitis and lymphadenitis occur, body temperature rises, and the general condition of the patient worsens. After epithelialization of erosions on the palms and soles, relapses of dyshidrotic eczema are manifested by the formation of already small bubbles under a thin stratum corneum. Occupational eczema results from skin contact with chemicals in a work environment. It usually develops after relapses of occupational allergic dermatitis, clinically no different from eczema of another origin. Nummular, or plaque, eczema occurs on the skin of the extremities, less often the trunk, where round, sharply limited from the surrounding skin, slightly raised erythematous plaques with a diameter of 1,5-3 cm or more are formed, consisting of closely grouped small papules, microvesicles and small erosions located on hyperemic skin. The edges of the plaques are finely scalloped with a narrow whitish border of the exfoliated stratum corneum (the result of the evolution of small bubbles formed along the edge). Within the plaques there is abundant fine-droplet weeping. As the severity of inflammation decreases, the exudate dries out to form serous crusts. The prevalence of rashes varies; a long, chronically relapsing course is typical. Eczematid is an abortive form of plaque eczema, it is characterized by the formation of round, oval and irregularly shaped pink spots of various sizes on the skin. Their surface is completely covered with bran-like and small-lamellar scales. Separate dotted serous crusts are found among the scales. When scraping the surface of the focus, small erosions are revealed, indicating hidden microvesiculation. The rash is usually accompanied by itching. The course is long. In unfavorable cases, the transformation of eczematid foci into typical nummular eczema is possible. In some cases, microbial eczema develops as a result of eczematization of chronic microbial or fungal skin lesions: streptococcal diaper rash, chronic diffuse streptoderma, infected wounds, fistulas, dyshidrotic form of mycosis of the feet, superficial candidiasis of the folds. At the same time, in the area of \uXNUMXb\uXNUMXbthe infectious lesion of the skin, rashes characteristic of eczema with small droplets of persistent weeping are formed. At the beginning, characteristic manifestations of a microbial (fungal) disease and eczema are simultaneously present in the lesion. In the future, eczematous phenomena increase, spread, while the symptoms of the initial bacterial (fungal) skin lesions gradually disappear. Paratraumatic eczema develops around wounds, trophic ulcers, fistulas. Varicose (or hypostatic) eczema develops on the shins in persons with varicose symptom complex. Dystrophically changed skin over varicose veins is more often affected. Mycotic eczema usually develops against the background of long-term mycosis of the feet (dyshidrotic and intertriginous forms). In its development, the combined effect of several exogenous (sensitization by metabolic products of fungi and pyococci, local antifungal drugs) and endocrine factors (atopy, vascular and endocrine disorders) is essential. Eczematous rashes first appear in the areas of localization of mycosis, and then gradually spread. Intertriginous eczema is eczema that occurs in large folds, perigenital and perianal areas. It develops as a result of eczematization of an intertriginous lesion due to the association of microbial and fungal microflora within the same focus. Treatment. In each specific case, it is necessary to establish which exogenous and endogenous factors have a significant impact on the reactivity of the skin, on the compensatory and adaptive mechanisms of the body. In cases where predominantly exogenous factors dominate, it is important to eliminate as much as possible exposure to the skin of various contact allergens, as well as simple irritants (irritants). If a patient has one of the forms of eczema, which is part of the group of a predominantly endogenous variant of the disease, in addition to the maximum protection of the skin from allergens and irritants, it is important to prescribe a treatment that is used for exacerbations of atopic dermatitis (antihistamines, sedatives, hypnotics, desensitizing agents). With microbial eczema, it is important to rationally influence the initial microbial (fungal) lesion, identify and normalize local disorders (microcirculatory, neurotrophic) in the regulation of the protective function of the skin. With widespread persistent eczema, short-term administration of small doses of a glucocorticosteroid drug is possible. When localizing foci on the limbs, reflex physiotherapeutic procedures are prescribed for the corresponding paravertebral nodes. External treatment is carried out taking into account the stage of eczema in the same way as patients with allergic dermatitis. The choice of forms and means of external therapy depends on the severity and characteristics of the inflammatory reaction of the skin. It should be borne in mind that with eczema, intolerance to both conventional pharmacological agents (including topical steroids) and indifferent medicinal bases often develops. In case of secondary infection and microbial eczema, the development of which was preceded by a pyococcal (mycotic) process in the skin, antimicrobial (antimycotic) agents should be used. In uncomplicated cases of eczema, short-term use of modern corticosteroid drugs with the highest safety index is justified. In some cases, combined preparations containing a topical corticosteroid and an antibiotic or antiseptic may be used. Author: Sitkalieva E.V. << Back: Leprosy >> Forward: Skin tumors (Epithelial tumors. Tumors of the skin glands and hair follicle. Neuroectodermal tumors. Tumors of mesenchymal tissue. Tumors of blood and lymphatic vessels)
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