Inflammatory reactions of the skin in response to exposure to environmental irritants. There are contact dermatitis and toxicoderma. Contact dermatitis occurs under the influence of the direct influence of external factors on the skin; with toxicerma, the latter initially penetrate into the internal environment of the body.
Etiology/pathogenesis
Irritants that cause dermatitis are of a physical, chemical or biological nature. So-called obligate irritants cause simple (artificial, artificial) dermatitis in every person. These include friction, pressure, radiation and temperature effects (see Burns and Frostbite), acids and alkalis, some plants (nettle, ash, caustic buttercup, spurge, etc.). Facultative irritants cause inflammation of the skin only in persons who are hypersensitive to them: allergic (sensitization) dermatitis occurs. The number of optional irritants (sensitizers) is enormous and continuously increasing. The greatest practical importance of them are salts of chromium, nickel, cobalt, formaldehyde, turpentine, polymers, medicines, washing powders, cosmetics, perfumes, insecticides, some plants (primrose, aloe, tobacco, snowdrop, geranium, garlic, etc.) .
The pathogenesis of simple dermatitis comes down to direct damage to skin tissue. Therefore, the clinical manifestations of simple dermatitis and its course are determined by the strength (concentration), duration of exposure and the nature of the irritant, and skin damage occurs immediately or shortly after the first contact with the irritant, and the area of damage strictly corresponds to the area of this contact.
Diagnosis
The diagnosis of simple dermatitis is based on a clear connection with exposure to an irritant, rapid onset after contact with it, sharp boundaries of the lesion, and rapid involution after removal of the irritant.
Symptoms
Simple dermatitis occurs acutely or chronically. There are three stages of acute dermatitis: erythematous (hyperemia and swelling of varying degrees of severity), vesicular or bullous (on an erythematous-edematous background, blisters and bubbles form, drying into crusts or opening with the formation of weeping erosions), necrotic (tissue decay with the formation of ulcerations and subsequent scarring). Acute dermatitis is accompanied by itching, burning or pain, which depends on the degree of damage. Chronic dermatitis, caused by prolonged exposure to weak irritants, is characterized by congestive hyperemia, infiltration, lichenification, cracks, increased keratinization, and sometimes skin atrophy. The clinical picture of allergic dermatitis is characterized by bright erythema with pronounced swelling. Against this background, numerous blisters and blisters may appear, resulting in weeping erosions upon opening. As the inflammation subsides, crusts and scales form, after which bluish-pink spots remain for some time. To confirm the diagnosis, allergy tests are used. Radiation dermatitis occurs in the same way, regardless of the type of ionizing radiation. Acute radiation dermatitis, which occurs from a single irradiation, less often during radiation treatment (radioepidermatitis), can be erythematous, vesiculobullous or necrotic, depending on the radiation dose.
Treatment
Eliminating the irritant. At the erythematous stage - indifferent powders and water-shaken suspensions. Bubbles, especially with abrasions, should be opened and treated with aniline paints. In the vesiculobullous stage - cold lotions (see Eczema). For all forms and stages, with the exception of ulcerative ones, corticosteroid ointments are indicated; for pyococcal complications, with disinfectant components. For chemical burns, first aid consists of immediate, copious and prolonged rinsing with water. Treatment of ulcerative necrotic lesions is carried out in a hospital setting.
Forecast
The prognosis is usually favorable, with the exception of necrotizing dermatitis of chemical and especially radiation etiology.
LECTURE No. 3. Atopic dermatitis
Atopic dermatitis (or diffuse neurodermatitis, endogenous eczema, constitutional eczema, diathetic prurigo) is a hereditarily determined chronic disease of the entire body with a predominant lesion of the skin, which is characterized by polyvalent hypersensitivity and eosinophilia in the peripheral blood.
Etiology and pathogenesis. Atopic dermatitis is a multifactorial disease. The model of multifactorial inheritance in the form of a polygenic system with a threshold defect is currently considered the most accurate. Thus, hereditary predisposition to atopic diseases is realized under the influence of provoking environmental factors.
An inadequate immune response contributes to increased susceptibility to various skin infections (viral, bacterial and mycotic). Superantigens of bacterial origin are of great importance.
An important role in the pathogenesis of atopic dermatitis is played by the inferiority of the skin barrier associated with impaired ceramide synthesis: the skin of patients loses water, becoming dry and more permeable to various allergens or irritants that enter it.
The characteristics of the psycho-emotional status of patients are essential. Characteristic features of introversion, depression, tension and anxiety. The reactivity of the autonomic nervous system changes. There is a pronounced change in the reactivity of blood vessels and the pilomotor apparatus, which is dynamic in nature in accordance with the severity of the disease.
Children who had manifestations of atopic dermatitis at an early age represent a risk group for developing atopic bronchial asthma and allergic rhinitis.
Diagnostics. To make the correct diagnosis, basic and additional diagnostic criteria are used. The criteria proposed at the First International Symposium on Atopic Dermatitis are used as a basis.
Basic criteria.
1. Itching. The severity and perception of itching may vary. As a rule, itching is more disturbing in the evening and at night. This is due to the natural biological rhythm.
2. Typical morphology and localization of rashes:
1) in childhood: damage to the face, extensor surface of the limbs, torso;
2) in adults: rough skin with an accentuated pattern (lichenification) on the flexor surfaces of the limbs.
3. Family or individual history of atopy: bronchial asthma, allergic rhinoconjunctivitis, urticaria, atopic dermatitis, eczema, allergic dermatitis.
4. The onset of the disease in childhood. In most cases, the first manifestation of atopic dermatitis occurs in infancy. This is often due to the introduction of complementary foods, the prescription of antibiotics for some reason, or climate change.
5. Chronic relapsing course with exacerbations in the spring and autumn-winter seasons. This characteristic feature of the disease usually appears no earlier than 3 to 4 years of age. A continuous off-season course of the disease is possible.
Additional criteria.
1. Xeroderma.
2. Ichthyosis.
3. Palmar hyperlinearity.
4. Follicular keratosis.
5. Increased level of immunoglobulin E in blood serum.
6. Tendency to staphyloderma.
7. Tendency to nonspecific dermatitis of the hands and feet.
8. Dermatitis of the breast nipples.
9. Cheilitis.
10. Keratoconus.
11. Anterior subcapsular cataract.
12. Recurrent conjunctivitis.
13. Darkening of the skin of the periorbital area.
14. Infraorbital Denny–Morgan fold.
15. Facial pallor or erythema.
16. White pityriasis.
17. Itching when sweating.
18. Perifollicular seals.
19. Food hypersensitivity.
20. White dermographism.
Clinic. Age periodization. Atopic dermatitis usually manifests itself quite early - in the first year of life, although its manifestation is possible at a later date. The duration of the course and the timing of remissions vary significantly. The disease can continue into old age, but more often its activity subsides significantly with age. There are three types of atopic dermatitis:
1) recovery up to 2 years (most common);
2) pronounced manifestation up to 2 years with subsequent remissions;
3) continuous flow.
Currently, there is an increase in the third type of flow. At an early age, due to the imperfection of the child’s various regulatory systems and various age-related dysfunctions, the effect of external provoking factors is much more pronounced. This may explain the decrease in the number of patients in older age groups.
In conditions of deteriorating environmental conditions, the role of external factors is increasingly increasing. These include exposure to atmospheric pollution and occupational aggressive factors, increased contact with allergens. Psychological stress is also significant.
Atopic dermatitis occurs with chronic recurrence. Clinical manifestations of the disease change with the age of patients. Long-term remissions are possible during the course of the disease.
The clinical picture of atopic dermatitis in children aged 2 months to 2 years has its own characteristics. Therefore, the infant stage of the disease is distinguished, which is characterized by the acute and subacute inflammatory nature of the lesions with a tendency to exudative changes and a certain localization - on the face, and with widespread lesions - on the extensor surfaces of the limbs, less often on the skin of the body.
In the vast majority of cases, there is a clear connection with nutritional stimuli. Initial changes usually appear on the cheeks, less often on the outer surfaces of the legs and other areas. Disseminated skin lesions are possible. The lesions are located primarily on the cheeks, in addition to the nasolabial triangle, the unaffected skin of which is sharply demarcated from the lesions on the cheeks. The presence of rashes on the skin of the nasolabial triangle in a patient with atopic dermatitis at this age indicates a very severe course of the disease.
The primary ones are erythematoedematous and erythematosquamous lesions. In more acute cases, papulovesicles, cracks, weeping, and crusts develop. Characterized by severe skin itching (uncontrollable scratching movements during the day and during sleep, multiple excoriations). An early sign of atopic dermatitis may be milky crusts (the appearance on the scalp of fatty brownish crusts, relatively tightly fused to the underlying reddened skin).
By the end of the first – beginning of the second year of life, exudative phenomena usually decrease. Infiltration and peeling of lesions increase. Lichenoid papules and mild lichenification appear. Follicular or pruriginous papules may appear, and rarely, urticarial elements. In the future, complete involution of the rash or a gradual change in morphology and localization is possible with the development of the clinical picture characteristic of the second age period.
The second age period (childhood stage) covers the age from 3 years to puberty. It is characterized by a chronically relapsing course, often depending on the season of the year (exacerbation of the disease in spring and autumn). Periods of severe relapses may be followed by long remissions, during which children feel practically healthy. Exudative phenomena decrease, pruriginous papules, excoriations predominate, and a tendency to lichenification, which increases with age. Eczema-like manifestations tend to cluster, most often appearing on the forearms and lower legs, resembling plaque eczema or eczematids. Erythematosquamous rashes around the eyes and mouth, which are difficult to treat, often appear. At this stage, typical lichenified plaques may be present in the elbows, popliteal fossae and on the back of the neck. Characteristic manifestations of this period also include dyschromia, which is especially noticeable in the upper back.
With the development of vegetative-vascular dystonia, grayish pallor of the skin appears.
By the end of the second period, the formation of changes typical for atopic dermatitis on the face is possible: pigmentation on the eyelids (especially the lower ones), a deep fold on the lower eyelid (Denny-Morgan symptom, especially characteristic of the exacerbation phase), in some patients - thinning of the outer third of the eyebrows. In most cases, atopic cheilitis is formed, which is characterized by damage to the red border of the lips and skin. The process is most intense in the area of the corners of the mouth. The part of the red border adjacent to the oral mucosa remains unaffected. The process never spreads to the oral mucosa. Erythema with fairly clear boundaries is typical; slight swelling of the skin and red border of the lips is possible.
After the acute inflammatory phenomena subside, lichenification of the lips is formed. The red border is infiltrated, peels off, and has multiple thin radial grooves on its surface. After the exacerbation of the disease subsides, infiltration and small cracks in the corners of the mouth may persist for a long time.
The third age period (adult stage) is characterized by a lesser tendency to acute inflammatory reactions and a less noticeable reaction to allergic irritants. Patients mainly complain of itchy skin. Clinically, the most characteristic lesions are lichenified lesions, excoriations, and lichenoid papules.
Eczema-like reactions are observed mainly during periods of exacerbation of the disease. Characterized by severe dry skin, persistent white dermographism, and a sharply enhanced pilomotor reflex.
Age-related periodization of the disease is not observed in all patients. Atopic dermatitis is characterized by a polymorphic clinical picture, including eczematous, lichenoid and pruriginous manifestations. Based on the predominance of certain rashes, a number of clinical forms of the disease in adults can be distinguished, such as:
1) lichenoid (diffuse) form: dryness and dyschromia of the skin, biopsy skin itching, severe lichenification, a large number of lichenoid papules (hypertrophied triangular and rhombic skin fields);
2) eczema-like (exudative) form: most typical for the initial manifestations of the disease, but in adults, skin changes such as plaque eczema, eczematid and eczema of the hands may predominate in the clinical picture of the disease;
3) pruriginous form: characterized by a large number of pruriginous papules, hemorrhagic crusts, excoriations.
Among the dermatological complications of atopic dermatitis, the first place is occupied by the addition of a secondary bacterial infection. In cases where staphylococcal infection predominates, they speak of pustulization. If the complication of the disease is caused primarily by streptococci, impetiginization develops. Sensitization to streptococci and eczematization of streptoderma foci often develop.
With prolonged existence of inflammatory changes in the skin, dermatogenous lymphadenopathy develops. Lymph nodes can be significantly enlarged and have a dense consistency, which leads to diagnostic errors.
Treatment. Therapeutic measures for atopic dermatitis include active treatment in the acute phase, as well as constant strict adherence to the regimen and diet, general and external treatment, and climatic therapy.
Before starting therapy, it is necessary to conduct a clinical and laboratory examination to identify factors that provoke exacerbation of the disease.
For the successful treatment of atopic dermatitis, detection and control of risk factors that cause exacerbation of the disease (triggers - nutritional, psychogenic, meteorological, infectious and other factors) are very important. The elimination of such factors significantly facilitates the course of the disease (sometimes to complete remission), prevents the need for hospitalization and reduces the need for drug therapy.
In the infant phase, nutritional factors usually come to the fore. Identification of such factors is possible with sufficient activity of the child’s parents (careful keeping of a food diary). In the future, the role of food allergens decreases somewhat.
Patients with atopic dermatitis should avoid foods rich in histamine (fermented cheeses, dry sausages, sauerkraut, tomatoes).
Among non-food allergens and irritants, dermatophagoid mites, animal hair, and pollen occupy a significant place.
Colds and respiratory viral infections can cause atopic dermatitis to worsen. At the first symptoms of a cold, it is necessary to start taking antisensitizing medications.
In young children, nutritional factors such as enzymatic deficiency and functional disorders are of great importance. It is advisable for such patients to prescribe enzymatic preparations and recommend treatment at gastrointestinal resorts. In case of dysbacteriosis and intestinal infections, targeted correction is also carried out.
For mild exacerbations of the disease, you can limit yourself to prescribing antihistamines. The most commonly used are new generation histamine H1 receptor blockers (cetirizine, loratadine), which do not have side sedative effects. Drugs in this group reduce the body’s response to histamine, reducing smooth muscle spasms caused by histamine, reducing capillary permeability, and preventing the development of tissue edema caused by histamine.
Under the influence of these drugs, histamine toxicity decreases. Along with the antihistamine effect, drugs in this group also have other pharmacological properties.
For moderate exacerbations of the disease, in most cases it is advisable to begin therapy with intravenous infusions of solutions of aminophylline (2.4% solution - 10 ml) and magnesium sulfate (25% solution - 10 ml) in 200 - 400 ml of isotonic sodium chloride solution ( daily, 6 – 10 infusions per course). In the lichenoid form of the disease, it is advisable to include atarax or antihistamines with a sedative effect in therapy. For an eczema-like form of the disease, atarax or cinnarizine is added to therapy (2 tablets 3 times a day for 7–10 days, then 1 tablet 3 times a day). It is also possible to prescribe antihistamines that have a sedative effect.
External therapy is carried out according to the usual rules - taking into account the severity and characteristics of inflammation in the skin. The most commonly used creams and pastes contain antipruritic and anti-inflammatory substances. Naftalan oil, ASD, and wood tar are often used. To enhance the antipruritic effect, phenol, trimecaine, and diphenhydramine are added.
In the presence of an acute inflammatory skin reaction with weeping, lotions and wet-dry dressings with astringent antimicrobial agents are used.
When the disease is complicated by the addition of a secondary infection, stronger antimicrobial agents are added to external remedies.
Externally, for mild and moderate exacerbations of atopic dermatitis, short courses of topical steroids and local calcineurin inhibitors are used.
The external use of drugs containing glucorticosteroids for atopic dermatitis is based on their anti-inflammatory, epidermostatic, coreostatic, antiallergenic, and local anesthetic effects.
In case of severe exacerbation of the process, it is advisable to carry out a short course of treatment with glucocorticosteroid hormones. The drug betamethasone is used. The maximum daily dose of the drug is 3–5 mg with gradual withdrawal after achieving a clinical effect. The maximum duration of therapy is 14 days.
For severe exacerbations of atopic dermatitis, it is also possible to use cyclosporine A (daily dose 3–5 mg per 1 kg of patient body weight).
Most patients in the acute phase require psychotropic medications. A long course of itchy dermatosis often provokes the appearance of significant general neurotic symptoms. The first indication for prescribing drugs that inhibit the function of cortico-subcortical centers is persistent night sleep disorders and general irritability of patients. For persistent sleep disturbances, sleeping pills are prescribed. To relieve excitability and tension, small doses of atarax are recommended (25–75 mg per day in separate dosages during the day and at night), a drug that has a pronounced sedative, as well as antihistamine and antipruritic effect.
The use of physical factors in therapy should be strictly individual. It is necessary to take into account the forms of the disease, the severity of the condition, the phase of the disease, the presence of complications and concomitant diseases. In the stabilization and regression phase, as well as as a prophylactic agent, general ultraviolet irradiation is used.
Prevention. Preventive measures should be aimed at preventing relapses and severe complicated course of atopic dermatitis, as well as preventing the occurrence of the disease in risk groups.
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Dermatitis is an inflammatory reaction of the skin in response to exposure to environmental irritants. The name “dermatitis” is used by many skin diseases, such as seborrheic dermatitis, atopic dermatitis, dermatitis herpetiformis, etc.
Clinical picture of dermatitis
The most common of these diseases are:Contact dermatitis and toxicoderma
For example, if an inflammatory reaction in the skin occurred when using a cream with some medicinal substance, then this is contact dermatitis, and if the same substance was given in tablets and a rash appeared on it, this is toxicerma.Simple contact dermatitis
The action of a strong irritant (for example, a burn, acid or alkali) causes simple inflammation - simple contact dermatitis. Simple contact dermatitis is caused by irritants: friction, pressure, radiation and temperature effects, acids and alkalis, substances of certain plants (nettle, hogweed).
In simple contact dermatitis, direct damage to skin tissue occurs. The manifestations of simple dermatitis and its course are determined by the strength and duration of exposure (for example, the degree of burns). Symptoms of simple contact dermatitis appear immediately or shortly after the first contact with the irritant, and the area of the lesion corresponds to the area of contact. Sometimes a chronic course of dermatitis is possible with prolonged exposure to the irritant.
Allergic dermatitis and eczema
Allergic dermatitis is based on an allergic reaction to a substance called an allergen. Allergic dermatitis, like other forms of allergies, occurs in individuals who are more or less predisposed to it.
Allergic contact dermatitis, unlike simple allergic contact dermatitis, does not develop immediately after contact with the irritant, and not on the first contact. For an allergic reaction (sensitization) to form, it takes up to several weeks from the first contact. Then, upon repeated contact, dermatitis develops. The area of change on the skin may extend beyond the contact area.
Acute manifestations of allergic contact dermatitis are also characterized by bright redness of the skin, erythema with pronounced swelling. Next, bubbles and even bubbles may appear, opening and leaving weeping erosions (wetting). The subsiding inflammation leaves crusts and scales. This complex is often called eczema.
Seborrheic and perioral dermatitis
Seborrheic dermatitis is a chronic inflammatory disease that affects those areas of the head and torso where the sebaceous glands are developed. Most often these are the borders of the scalp, forehead, cheeks and nasolabial folds. Dandruff is often considered a mild or early form of seborrheic dermatitis.
The cause of dandruff and seborrheic dermatitis is most often considered to be a complex of factors leading to the proliferation of yeast fungi of the genus Malassezia on sebum-rich skin. These fungi are excreted from the skin of most people. Normally, these are harmless inhabitants of the skin - commensals. Therefore, the disease cannot be considered purely infectious, since almost all of us carry these fungi on ourselves.
Under certain conditions, the body loses the ability to control the growth of Malassezia. The reproduction and activity of fungi leads to increased peeling of the skin.
Atopic dermatitis
A very complex disease, a chronic and genetically determined inflammatory skin lesion of an allergic nature. It can be caused by several or even many factors - allergens, and not only contact ones, but also those coming in through inhalation (pollen, dust) or from food (food allergies). Thus, atopic dermatitis is not strictly contact by definition.
Atopic dermatitis usually develops in early childhood and resolves soon, but can remain lifelong. Synonyms for atopic dermatitis in adults are neurodermatitis and eczema, and in children - diathesis.
The cause of an allergic skin reaction can also be triggered by internal factors:
- disturbances in the functioning of the gastrointestinal tract (dysbacteriosis, constipation, digestive disorders, etc.);
- liver diseases (hepatitis, cholecystitis, etc.);
- chronic infectious diseases;
- hormonal disorders;
- various skin diseases;
- taking a number of medications.
Dermatitis, treatment
Treatment of dermatitis is prescribed by a dermatologist and comes down primarily to identifying the allergen, conducting a detailed survey of the patient about the peculiarities of his work, a thorough analysis of the medical history and identification of possible etiological agents. In the treatment of dermatitis, both local and general medications are used.Dermatitis, prevention
- compliance with safety regulations at work and at home;- timely sanitation of focal infections and mycoses of the feet;
- use of antibiotics and other sensitizing medications strictly according to indications, taking into account their tolerability in the past.
DERMATITIS.
This is an acute inflammation of the skin caused by exposure to
physical, chemical and biological irritants. Depending
Depending on the nature and mechanism of development of the process, stimuli are divided
to:
1) obligate - when exposed to the skin, regardless of the individual,
will definitely cause irritation (concentrated mineral acids); under
Their influence always develops simple contact dermatitis.
2) optional - dermatitis in persons with increased
sensitivity to irritants - allergic contact dermatitis.
D-D simple contact dermatitis and allergic:
With contact dermatitis, erythema develops, accompanied by
the appearance of papular and vesicular elements - erosion - weeping,
when infection is attached - the appearance of secondary morphological
elements: erosion, scales, crusts.
Clinically:
1) for contact - clarity of the boundaries of the damage (the lesion repeats
form of stimulus); allergic - the boundaries are blurred, the focus goes beyond
limits of contact, rashes may appear at a considerable distance
from the place of irritation;
2) with contact - monomorphic rash, with allergy. - polymorphic;
3) with contact - when the irritant is eliminated, there is a quick cure;
4) with contact - never recurs;
5) subjective: during contact - pain, burning, in the resolution phase -
itching; with allergies - itching of varying intensity (treatment is necessary
include hyposensitizing antihistamines).
Treatment.
External therapy:
a) pastes: zinc + 3-5% naphtholan, 3% tar, 5% dermatol,
b) sinolar, flucinar,
c) for weeping - treatment begins with silver nitrate lotions
0.25%, furatsilin, rivanol 1:500, 2% boric acid solution, tannin 2-3%,
TOXICODERMIA.
This is damage to the skin that develops under the influence
irritating factors that are delivered hematogenously.
The factors are:
Exogenous
a) food;
b) medications;
c) household and industrial;
Endogenous
a) unusual metabolic products;
b) ordinary--//--//--//--, in case of their excessive accumulation.
The basis of the disease is sensitization of the body, aggravated
allergy history.
General characteristics:
1) begins acutely;
2) often the onset is accompanied by a violation of the general condition;
3) profuse, symmetrical monomorphic rash.
The following forms of primary and secondary morphological are distinguished:
elements: macular, papular, vesicular, bullous,
pustular, erythrodermic.
Spotted:erythematous spots with clear boundaries, hemorrhages,
hyperpigmentation. Erythematous spots - of varying sizes, with
resolution resemble one-time lichen. Toxic melasma -
accompanied by damage to the internal organs, a dim
erythema, then slate-gray spots appear against its background, then
nodules and telangiectasia.
Papular:often hemispherical d=2-5 mm, sometimes polygonal
flat with a central recess, reminiscent of lichen ruber, but
lesion on the extensor surfaces.
U evil: the walls of blood vessels are predominantly affected, most often on
lower extremities. Fixed erythema occurs on the same
place, pigmentation intensifies.
Acute epidermal necrolysis (Lyell's b.): basically allergic
mechanism, in the past - an allergic reaction to medications. Disease
begins acutely, accompanied by high t, headache,
dizziness, vomiting, sometimes it can proceed as usual
toxicerma, then the process becomes diffuse, appears
painful erythema, as a result of necrotization the epidermis slides,
exposing a bright red shiny surface (reminiscent of a second burn
degrees). The general condition is severe: t = 38-39, general intoxication,
loss of consciousness, inhibition of gastrointestinal glands, blood thickening, 20-30% lethal.
Diagnostics:
1) medical history;
2) clinic;
3) changes in the blood (toxic granularity of leukocytes
at c. Lyella)
4) tube samples.
Treatment:
1) cessation of antigen supply;
2)drink plenty of water;
3) diuretics and laxatives;
4) antihistamines 1 tablet 3 times a day, change every week
drug;
5) in case of severe form, large doses of glucocorticoids (in case of Lyella
80-100 mg);
6) detoxification therapy: hemodez, reopolyglucin every other day
400 ml;
7) external therapy - under the frame (as with a second-degree burn);
ECZEMA.
This is a chronic relapsing neuro-allergic disease
nature, characterized by serous inflammation of the upper layers of the dermis,
focal spongiosis of the spinous layer of the epidermis, accompanied
polymorphous rash and severe itching.
1808-Willen isolated eczema from numerous diseases.
Etiology and pathogenesis:
Factors - neurogenic, allergic.
For the neurogenic factor they say:
Presence of itching;
Symmetrical localization of rashes;
The first manifestation after nervous tension or psychological trauma;
When the nerve trunk is compressed - eczema below the scar, after
eliminating the scar - resolving the process;
Around the lesion, there is a violation of tactile, temperature,
pain sensitivity;
Positive effect after prescribing electrosleep,
acupuncture, sedatives.
For an allergic factor they say:
The presence of increased sensitivity to a number of irritants -
polyvalent sensitization;
Combination with bronchial asthma, allergic rhinitis;
Violation of the immunological status;
Due to a violation of the central nervous system - a violation of trophism - in the skin
foreign products are formed - antibodies are formed -
autoimmunization - high titers of antibodies are formed against one’s own
skin;
Background purulent infection;
Dysfunction of the gastrointestinal tract - impaired membrane permeability - into the blood
incomplete protein breakdown products - allergens - enter.
Disruption of the functions of the endocrine glands - the creation of prosperous
conditions for the development of sensitization.
Shapes:
1) true (endogenous)
Flurigenous;
Dyshidrotic;
Hyperkeratotic;
2) microbial
Coin-shaped
3) seborrheic
4) professional
5) children's
A serious complication of eczema is the attachment of herpetic
infections - herpetic eczema or Kaposi's eczema develops.
TREATMENT.
1) elimination of functional disorders of various organs and systems;
2) electrosleep, acupuncture, hypnotherapy, bromine preparations,
valerian root, tranquilizers, antihistamines;
3) hyposensitizing (pr-you Ca, Na THIOSULPHATE);
4)vitamins B1, B6, B12, IM, P;
5) immunocorrectors and immunomodulators (T-activin, levomisol 0.1 - 1 time
2 days, methyluracil 0.5 - 3 times 3 weeks);
6) adaptogens;
7) injections of gammaglobulin, histoglobulin - 3 ml subcutaneously every other week,
for a course of 6-8 injections; repeat the course after 3-4 weeks, without
8) if previous measures are ineffective, hemosorption is carried out,
glucocorticoids, adrenal stimulants;
9) dairy-vegetable diet;
10) external therapy:
Ural Federal District;
Laser therapy;
Electrophoresis;
Baths with pine extracts. Bath duration is 15-20 minutes,
t= 37-38, an hour before bedtime, lubricate the lesions
For weeping lesions - lotions (2% boric, 2% resorcinol, 0.25%
lapis, rivanol 1:1000);
Pastes: zinc, Lassara, with the addition of naphthalan, tar,
urea 2-15%; increase concentration weekly;
Glucocortoid ointments.
Dermatitis means inflammation of the skin, but dermatologists use this term to define a special group of inflammatory skin diseases. Clinically, they manifest themselves as more or less clearly defined erythema, usually accompanied by itching. Lesions go through 3 stages - acute, subacute and chronic. Primary elements are spots, papules, vesicles, edematous spots, plaques; secondary - crusts, scales, cracks and lichenification. Primary histological changes are characterized by spongiosis (intercellular epidermal edema), the presence of lymphocytes or eosinophils in the dermis and epidermis.
DERMATITIS- arises as a result of the direct influence of external factors on it. There are simple contact and allergic dermatitis.
SIMPLE DERMATITIS occur in all people when the skin is exposed to obligate (obligatory) irritants, which can be chemical (concentrated mineral acids, alkalis, boiling water), physical (UV rays, high and low temperatures, etc.), biological (hogweed), mechanical ( friction, prolonged pressure). The severity of inflammatory phenomena depends on the strength of the irritant and the time of its exposure to the skin, and therefore, in the development of simple dermatitis, 3 stages (forms) are distinguished: erythematous, vesiculobullous and necrotic-ulcerative. Inflammatory changes in area strictly correspond to the site of exposure to the stimulus and occur without a latent period. Simple dermatitis, both at work and at home, often develops as a result of an accident (burns, frostbite).
ALLERGIC DERMATITIS occur under the influence of facultative irritants (sensitizers) in persons with hypersensitivity to them and pathogenetically represent a delayed-type allergic reaction. Most often, allergic dermatitis develops as a result of repeated exposure of the skin to synthetic washing powders, cosmetics, medications, chromium, nickel, etc. Skin changes with allergic dermatitis, unlike simple dermatitis, occur after a latent period, which ranges from 7-10 days to a month and longer. The clinical picture of allergic dermatitis is similar to that of acute eczema, and therefore, in its course, erythematous, vesicular, weeping, cortical and squamous stages are distinguished. The process is accompanied by itching. Inflammatory phenomena can extend beyond the skin area where the irritant is applied. Diagnosis of simple dermatitis usually does not cause difficulties due to the absence of a latent period between exposure to the irritant and the occurrence of typical skin changes. When diagnosing allergic dermatitis, the localization of the lesion (usually open areas of the skin of the hand, face) and the eczema-like nature of the inflammatory changes in the skin are taken into account. Often, to confirm the diagnosis, they resort to allergic skin tests, which are mandatory when identifying an occupational sensitizer (occupational dermatitis).
Treatment
: for simple and allergic dermatitis, the main elimination of the action of the irritant. For simple dermatitis in the form of chemical burns from concentrated acids and alkalis, the emergency remedy is long and abundant rinsing with water. For severe erythema with edema, lotions and corticosteroid ointments are indicated; for vesiculobullous rashes, the blisters are opened, followed by the application of disinfectant cold lotions, as well as ointments with corticosteroids and antibiotics (Lorinden C, celestoderm with garamycin, etc.). Treatment of patients with necrotic-ulcerative manifestations is carried out in a hospital, and with allergic dermatitis according to the principles of treatment of acute eczema.
PELLAGROID DERMATITIS- dermatitis that develops under the influence of insolation in people who abuse alcohol and suffer from liver diseases. The disease is similar to pellagra. The lesions are characterized by symmetrical diffuse erythema with swelling on the forearms, dorsum of the hands, face, and neck. Unlike pellagra, there is no skin atrophy, damage to the mucous membranes, or general severe phenomena.
Treatment
: exclusion of alcohol, correction of liver disorders. Nicotinic acid, xanthinol nicotinate, vitamins B, B1, B3, B5 are prescribed in normal doses, and photoprotective ointments are prescribed locally (Shield, Luch). In the acute period, lotions with a 1-2% solution of amidopyrine, resorcinol, tannin, etc., and corticosteroid ointments are indicated.
PERIORAL DERMATITIS- a disease of the facial skin caused by opportunistic microflora due to an increase in its quantity and a change in its qualitative composition. It occurs predominantly in women, often young and middle-aged. Predisposing factors are the use of corticosteroid ointments for acne vulgaris, seborrheic and drug dermatitis, rosacea; thinning of the epidermis; foci of chronic infection, severe infectious diseases; dysfunction of the digestive tract, hormonal dysfunction, taking contraceptives. In the pathogenesis of the disease, a large role is given to the inhibition of local mechanisms of antibacterial resistance of the facial skin, a decrease in the general resistance of the body, an increase in the tension of cellular and (or) humoral immunity, including to bacterial allergens; hormonal imbalance. The skin lesion is characterized by non-follicular, 1-2 mm in diameter hemispherical papules from pale pink to bright red and single waxy, shiny translucent pseudopustules. Papules do not tend to grow, do not merge, are often located in isolation or are grouped into poorly defined small lesions, the surface of which is often covered with whitish translucent scales. Erythema and teloangiectasias are not always found. The rash is localized only on the skin of the face, without affecting other areas, including the neck. There are 3 localization options: perioral, periorbital and mixed. The diagnostic feature is a narrow, 2-3 mm in diameter, rim of unaffected, paler skin around the red border of the lips. Subjective sensations are usually absent. The onset of the disease is nonspecific, development is usually rapid, the course is monotonous, and there are no stages.
The diagnosis is usually not difficult. It is necessary to differentiate from rosacea, seborrheic dermatitis, acne vulgaris, pyoderma.
Treatment
: cancellation of corticosteroid ointments with subsequent relief of the “exacerbation reaction” that occurs 5-10 days after their discontinuation. Clinical manifestations of “withdrawal dermatitis” are characterized by bright red erythema, sometimes significant swelling of the entire facial skin, an increase in local temperature, an increase in the number and area of rashes, and the appearance of subjective sensations in the form of a sharp burning sensation, itching, and skin tightness. The duration of “withdrawal dermatitis” is 7-10 days, its treatment includes a hypoallergenic diet, desensitizing and diuretic drugs, topical herbal lotions and indifferent creams or oil: the use of cosmetics and soap is not recommended. Then tetracycline is prescribed in medium doses (if perioral dermatitis occurs against the background of seborrheic skin changes), metronidazole according to a permanent regimen (if perioral dermatitis is combined with rosacea or diseases of the gastrointestinal tract), decaris, methyluracil, biogenic stimulants, antihistamines, vitamins , belloid (for severe neurotic disorders). Locally, alternating lotions of herbal infusions (chamomile, string, sage, nettle) with pastes with 2-5% naphthalan and tar are used; for increased dryness, indifferent creams with olive or peach oil. In the case of a combination of perioral dermatitis and demodicosis, acaricidal agents are prescribed. Cryomassage with carbonic acid snow or liquid nitrogen is also used in courses (2-3) of 10-12 sessions per course. At the same time, concomitant pathology is identified and corrected.
SEBORRHICAL DERMATITIS inflammatory dermatosis in infants. Develops in the 1st month of life, often at the end of the 1st week and the beginning of the 2nd; lasts for 3-4 months, then regresses. There are 3 degrees of severity of the process: mild, moderate and severe. The disease begins with hyperemia and slight infiltration of the skin folds (behind the ear, cervical, axillary, inguinal-femoral) with dissemination of scaly maculopapular elements of a numular nature along the periphery of the lesions (mild degree), which makes it necessary to differentiate dermatitis from psoriasis. The process of moderate severity extends beyond the boundaries of the skin folds, involving large areas of smooth skin on the scalp. Characterized by erythema, infiltration, peeling. Minor dyspeptic disorders are typical: regurgitation 3-4 times a day, loose stools. In severe forms, at least 2/2 of the skin is affected; on the scalp there is a “bark” of fatty scales against a background of erythema and infiltration of the skin. Dyspepsia and slow weight gain are also characteristic. The condition is very close to that of desquamative Leiner-Moussou erythroderma, but regresses faster (lasts 3-4 months). Complications such as otitis media, anemia, and pneumonia are possible.
Treatment : for mild cases, only external treatment is indicated: 2-3% naphthalan, ichthyol ointments; for moderate and severe cases, antibiotics are prescribed (for 10 days), blood transfusions, plasma transfusions, glucose with ascorbic acid, vitamins A, C, group B.
SCHISTOSOMIC DERMATITIS (cercarial dermatitis, swimmer's itch, water scabies) - acute inflammation of the skin, predominantly urticarial in nature. It occurs in humans upon contact with cercariae of the larval stage of some adult helminths, usually found in polluted water bodies. The causative agents are usually the larvae (cercariae) of schistosomes of waterfowl (ducks, gulls, swans) and, less commonly, some mammals (rodents, muskrats, etc.), which, having penetrated the thickness of human skin, die before reaching puberty. The disease often occurs in tropical countries of Africa and Asia, and rarely in Russia. Human infection usually occurs through swimming or working in ponds, swampy, stagnant or slow-moving bodies of water contaminated by the feces of infected birds, mammals or people. When a person comes into contact with cercariae, they attach to the skin and quite quickly, with the help of a special biting apparatus, penetrate into the thickness of the skin. Further migration of cercariae in the skin is facilitated by the lytic effect of the secretion they secrete. The clinical picture of schistosome dermatitis is characterized by some variability and depends on the immunobiological state of the body, the intensity and duration of contact with cercariae. When the cercariae penetrate the skin, patients feel severe pain. After a few minutes or 1-3 hours, the feeling of pain turns into intense itching. At the same time, erythematous spots appear at the sites of cercariae penetration, which turn into blisters the size of beans. As exudation increases, bubbles containing a clear opalescent liquid appear on the blisters. In the case of pyococcal infection, blisters can transform into pustules (in weakened people, especially children, ecthyma may develop). In most cases, after 4-5 days the severity of the inflammatory phenomena decreases, and after 10-14 days the process resolves without a trace. Cases of the development of diffuse hyperemia involving almost the entire skin (schistosomal erythroderma) have been described. Histologically, in the epidermis around the site of penetration of cercariae into the skin, swelling, local lysis of epithelial cells and the presence of intraepidermal “passages” filled with neutrophils and eosinophils are noted; in the dermis there is an infiltrate consisting of polymorphonuclear leukocytes and lymphocytes. The diagnosis is made based on the typical clinical picture and history. Treatment is mainly symptomatic: lotions, itching talkers, creams, ointments. It is also advisable to prescribe desensitizing and detoxifying agents (diphenhydramine, calcium chloride, sodium thiosulfate), drinking plenty of fluids, and in case of pyococcal infection, antibiotics. Preventive measures are limited to the destruction of mollusks and rodents. As a personal protective measure, it is recommended to lubricate the skin with 40% dimethyl phthalate ointment before bathing, and dry thoroughly with a towel after bathing.
