Eczema

ECZEMA, eczema (from Greek ekzeo - I boil). The term was first established in relation to a specific group of skin diseases by the English physician Willan (R. Willan), who noted 4 forms of eczematous processes (eczema impetiginosum, eczema rubrum, eczema solare, eczema mercuriale). Such a division is of course incorrect, as certain diseases that are in essence not eczema but dermatitis (solar, mercury dermatitis) were included in E. Subsequently, Rayer proposed to exclude from the group of eczematous processes diseases that do not belong to E. Devergie establishes the following cardinal signs for skin diseases belonging to E.: redness, itching, secretion of rapidly drying fluid, and the presence on the skin surface of tiny pits that secrete fluid. More precise indications about the nature of the eczematous process are given by F. Hebra, who studied in detail the inflammation of the skin caused by applications of croton oil. By comparing the data from these experiments with the occurrence and course of natural E., Hebra establishes the division of the eczematous process into 5 basic forms: 1) eczema squamosum, 2) eczema papulosum, 3) eczema vesiculosum, 4) eczema rubrum, 5) eczema impetiginosum. Subsequently, Kaposi, while generally following Hebra's division, introduces a number of clarifications, noting that the initial symptom of developing E. is redness, and that peeling represents the final stage of eczema. The general course of the eczematous process, according to Kaposi, comes down to the following periods: 1) redness of the skin (eczema erythematosum), 2) formation of small nodular elements (eczema papulosum), 3) formation of vesicles (eczema vesiculosum), 4) weeping (eczema madidans, s. rubrum), 5) formation of crusts (eczema crustosum), and with secondary infection by pyogenic cocci - eczema impetiginosum, 6) peeling (eczema squamosum). Such a division is generally preserved to the present time. However, it should be borne in mind that the eczematous process does not always go through all stages; in some cases, the process does not progress to weeping, and the vesicles that appear quickly dry into crusts, under which epithelialization and subsequent peeling occur, which concludes the eczematous process; in some cases, following the initial redness, the process begins to reverse: the redness disappears and sequential peeling appears, etc. Usually, the eczematous process is also characterized by its location in the form of separate foci, single or multiple, often of irregular configuration, sometimes with a tendency to peripheral growth. In its course, E. can quickly undergo reverse development, and sometimes it gives exacerbations or has a tendency to a prolonged course, which is why acute and chronic forms are distinguished. In general, the clinical manifestations of E. are very close to the clinical picture of certain dermatitis caused by external agents physically and chemically harmful to the skin, which is why it is not always possible to draw a sharp line between E. and dermatitis. Such dermatitis, to distinguish them from true eczema, Besnier proposes to consider as "eczematization" of the skin. Darier introduces some additional terms into the doctrine of E.: he proposes to call "eczematoses" those chronic diseases that other authors called "diathetic eczema," and "eczematids" certain forms of dry eczematous processes, seborrheic E. ("seborrheids" of other authors). The symptomatology of E. depends to a large extent on the nature of the inflammatory phenomena of the superficial layers of the skin, the degree of intensity of the process, the stage of development, localization, individual characteristics of the patient, etc. The first clinical sign of developing E. is redness of the skin, which usually appears in the form of separate points that quickly merge with each other, forming what might be called an erythematous reddening of the skin. Sometimes this redness appears from the very beginning as diffuse, although such redness is usually characteristic of dermatitis from external, skin-irritating causes. At this stage, the eczematous process can stop in its development and subsequently undergo reverse development with subsequent peeling (often parakeratotic) of the epidermis. In some cases, against the background of erythematous redness, tiny papules quickly arise, usually located in the openings of the skin follicles (ecz. folliculare), or small vesicles (ecz. vesiculosum), which subsequently dry with the formation of crusts or increase in size to that of a hemp seed and partially merge with neighboring ones. The content of the vesicles is clear serous fluid; sometimes it subsequently becomes cloudy or even purulent, which usually depends on secondary infection by pyogenic bacteria. The multicameral nature of the vesicles is often noted, indicating the merging of several vesicles. At this stage, the process can stop, and the vesicles dry into crusts (eczema crustosum, or impetiginosum when pustules dry), under which epithelialization occurs with subsequent falling off of crusts and peeling of the epidermis (eczema squamosum). If the vesicles lose their cover under the influence of excessive pressure of fluid or from scratching, then the red, horny layer-free epidermis is exposed, constantly secreting serous fluid surface (eczema madidans, s. rubrum). This stage is the highest degree of the eczematous process, and here too the process subsequently stops with the formation of crusts and subsequent peeling. In general, in E., different stages of development are usually noted, and not only in different foci, but often in the same focus, a difference can be noted in the central and peripheral parts in terms of the predominance of certain primary elements (polymorphism of the elements of the rash).-Itching is a constant companion of eczematous processes, and its degree varies in different cases. Constant scratching can lead to both exacerbation of the process and the possibility of secondary infection by pyogenic bacteria. Acute E. (eczema acutum) usually arises quickly in the form of redness with a feeling of burning and itching, formation of vesicles and weeping, and the clinical picture, depending on the degree of intensity of the process and its localization, can give various varieties, but in general the process quite quickly stops at one stage or another and ends within a few weeks with reverse development. Chronic E. (eczema chronicum) develops as a result of acute E. that has taken a prolonged course, or it develops from the very beginning without preceding acute phenomena. In it, manifestations characteristic of acute E. may occur (especially during exacerbations), although more often under the influence of the duration of the inflammatory process and constant scratching, a more or less pronounced infiltration of the skin with thickening of the epidermis develops, and the skin surface takes on a shagreen-like character with sharply expressed skin fields and deepened grooves (lichenification) [see separate table (art. 399-400), fig. 4]. The localization of E. also determines some characteristic features of the eczematous process. Thus, on the hairy part of the head, the formation of vesicles is rarely seen, but crusts usually quickly form, sometimes gluing the hair into a felt-like mass (tinea-plica polonica); on the skin of the face, in addition to the usual forms of acute and chronic E., sometimes acute E. is noted, accompanied by marked hyperemia and edema, resembling erysipelas. The auricles in acute E. are often thickened, and the auditory canal is narrowed; behind the auricles, a fissured weeping surface along the postauricular fold. Along the edge of the eyelids - manifestations of blepharitis, sometimes with the appearance of pustules in the follicular openings, accompanied by temporary or permanent loss of eyelashes. On the red border of the lips, crustose or lamellar forms are observed (pityriasis labiorum, eczema exfoliativum); in the corners of the mouth, eczematous phenomena are accompanied by the formation of cracks, and with secondary infection, the process can take on the character of angulus infectiosus with clouding and hyperplasia of the epidermis. In E., in the area of the mustache and beard, a mass of pustules often appears in the follicular openings (eczema sycosiforme). In the area of the eyebrows, drier, peeling forms of E. are more common. E. of the neck is more often located on the lateral and posterior surfaces (and in children on the anterior surface of the neck folds), often giving lichenified forms here. Primary eczematous foci are rarely noted on the trunk. E. is often noted in the area of the breast nipples, especially in breastfeeding women. In the area of the genital organs, E. is often encountered, usually affecting in men the scrotum, the perineal area, or in the area of the inguinal-genital folds in both sexes, and here under the irritating effect of sweat, diaper rash easily appears, and subsequently eczematous phenomena develop (eczema intertriginosum). Here too, eczematous lesions (with sharply defined borders) caused by a fungus (Epidermophyton inguinale) are often noted, known under the name eczema marginatum (borderline E.).

Eczematous lesions are not uncommon around the anus, accompanied by severe itching and the formation of cracks. Here, phenomena of lichenification are often observed, sometimes with whitish areas surrounded by a zone of hyperpigmentation (neurodermitis alba). On the upper extremities, the favorite localization of E. is the flexor surfaces (especially the elbow flexures), although the extensor surfaces may also be affected, and sometimes the process is localized only in the elbow areas, usually in the form of lichenized foci. On the hands, the lesion is usually localized on the dorsal surface, often in the form of limited foci (more often in the area between the metacarpal bones of the thumb and index finger), simulating a mycotic skin lesion with sharply defined borders. On the palmar surface of the hands, eczematous lesions are rare. Here there is sometimes a special form of E., characterized by phenomena of marked thickening of the horny layer and the formation of deep cracks (eczema tyloticum). In addition, on the lateral surfaces of the fingers and palmar surfaces, eczematous complications of dyshidrosis (eczema dysidroticum) or focal, sharply limited eczematous areas may occur, sometimes in a semilunar or sickle shape, partly resembling dyshidrotic phenomena (eczema pseudodysidroticum), and in most cases such foci turn out to depend on a fungal skin lesion (eczema mycoticum). In some cases, such a skin lesion must be considered as 'mykid,' depending on a fungal lesion of the feet, because when the feet are treated, the foci on the hands disappear spontaneously, whereas without treatment of the feet, these foci may sometimes exacerbate, sometimes improve and persist, stubbornly resisting local therapy; in some cases, such foci give sharp exacerbations when compresses are applied to the affected areas of the feet. On the lower extremities, in general, the nature of eczematous manifestations corresponds to the same type as on the upper extremities. It should be borne in mind that on the feet, mycotic E. are often found, usually depending on the fungus Epidermophyton inguinale, with a favorite localization in the interdigital and subdigital folds and spreading to the dorsal surface of the feet and further to the area of the arch of the foot, simulating here a dyshidrotic process with the formation of vesicles and large blisters. In the area of the nail folds, eczema is often accompanied by the development of paronychia, sometimes with separation of the nails. From the side of the nails, peculiar changes are also noted, which, according to Unna, depend on a lesion of the nail bed: at the free end of the nail and on the lateral folds, thickening and loosening appear, spreading over the entire surface of the nail, which becomes dull and easily crumbles and disintegrates layer by layer. In some cases, the eczematous process spreads to large areas of the body, giving in different areas one or another peculiarities (in places in the form of dry scaling, and in the flexures weeping E.), and sometimes a general E. also develops, accompanied by a number of general phenomena (feeling of chill, insomnia, febrile condition, etc.). The etiology of E. has not yet been clarified. A number of experiments by various authors with methods of various skin irritations speak for the special sensitivity of the skin to external irritating factors in eczematous patients and for the possibility of inducing increased skin sensitivity in healthy individuals by repeating skin irritations, and this increased sensitivity may manifest itself only to the same irritant (monovalent sensitization) or to various irritants (polyvalent sensitization). This sensitization of the skin can be either local (at the sites of former irritations) or general-over the entire skin surface of the body. Bloch found that the skin of eczematous patients is 7 times more sensitive to external irritants than the skin of healthy individuals, i.e., the skin of eczematous patients is in a special state of readiness to react to the slightest external irritants (Eczembereitschaft). The fact that even with internal administration of preparations (which give eczematous skin inflammation with their external application) it is possible to obtain eczematous phenomena speaks for the possibility of the appearance of E. from various internal causes (autointoxication). The symmetrical arrangement of eczematous foci speaks for an internal cause, probably acting through the nervous system. Ultimately, for the occurrence of E., two conditions are required: 1) predisposition (congenital or acquired) and 2) a cause that can give an eczematous skin lesion. Predisposition to E. may depend on various causes (various general diseases and metabolic disorders, such as obesity, uric acid diathesis, diseases of the digestive tract, arthrism, bronchial asthma, disorders of the activity of the endocrine glands, etc.). The producing cause can be various external irritants, often depending on the influence of the profession (light, temperature, water, various chemical preparations, mechanical irritations), then bacterial and fungal skin lesions, etc., as well as some internal causes (internal administration of medications, poor-quality food, preserves, various marinades, cheese, etc.).- Pathological anatomy of E., depending on the nature of the eczematous lesion, gives various histological pictures, but in general changes are noted in the epidermis and superficial layers of the skin. In the epidermis-phenomena of spongiosis and formation of vesicles, loss of the horny layer, acanthosis, parakeratosis; in the skin itself-edema of the papillae, hyperemia of the papillary and subpapillary layers, perivascular infiltration. Diagnosis of E. is based on the characteristic features of clinical manifestations of superficial skin inflammation in the presence of phenomena of polymorphism, localization, itching, and data from the anamnesis. The acute erythematous form of E. (usually of the face) is easily distinguished from erysipelas by the absence of sharply defined borders, pain on pressure, and elevated temperature. Polymorphous exudative erythema, with its characteristic efflorescences, characteristic localization, and course, is also easily distinguished from E. Duhring's disease, accompanied by polymorphism of the elements of the rash, having a tendency to group arrangement, its course, absence of diffuse skin lesion, can also without difficulty be distinguished from E. Contagious pustular rash differs from impetiginous E. by the presence of characteristic crusts resembling candied honey, sharp borders, tendency to appear new foci of lesion, absence of diffuse inflammatory condition of adjacent parts of the skin. Chronic squamous E. can hardly be confused with other skin diseases accompanied by scaling (psoriasis, parapsoriasis, lupus erythematosus, epidermophytoses, etc.). In the diagnosis of E., for the purposes of rational treatment, it is also necessary to decide whether we are dealing with primary E. or with secondary, depending on the presence of other pathological processes of the skin and being their complication (scabies, pediculosis, other itchy dermatoses). Treatment of E. is carried out in two directions: causal treatment and local treatment of the eczematous lesion. If the cause of E. is a harmful local influence of physical or chemical agents, then elimination of the harmful agent and prescription of local indifferent means is often sufficient for the cure of E. In some cases, where the causal factor lies in the patient's profession, it is necessary to raise the question of changing the profession. If there is reason to associate E. with the general state of health (diabetes, uric acid diathesis, disorders of the activity of the digestive tract, etc.), then, of course, along with local treatment, it is necessary to treat the underlying disease. There are no special remedies for the general treatment of E., however, some preparations may have a beneficial effect on cases of persistently recurrent or chronic E. The widest application is given to arsenic preparations internally in the form of Fowler's solution, or in the form of pills (e.g., 'Asian'), or else in the form of subcutaneous injections, and treatment with arsenic must be carried out persistently, observing the required dietary regimen. Calcium chloride is often prescribed internally (0.5 three times a day or a 10% solution). Intravenous infusions of sodium bromide, calcium chloride, or sodium thiosulfate are used. Further, in some cases, success has been noted with autogenous blood therapy, nonspecific protein therapy, etc., as well as with organotherapeutic preparations according to indications of possible etiological factors. Local treatment of E. must be carried out depending on the form and degree of inflammatory phenomena. Due to the easy irritability of the skin, washing with soap should be avoided, and in severe phenomena, washing should be completely abandoned, using for cleansing the skin some vegetable oil, purified gasoline, or 60% alcohol. In less severe inflammatory phenomena, a weak solution of boric acid, borax, or Burow's solution can be used, preferably with an admixture of glycerin. Various disinfectant solutions and ether irritate.

In fresh inflammatory phenomena, indifferent powders (talc, starch, possibly with an admixture of zinc oxide) or lotions (zinc oxide, talc, glycerin, distilled water—all in equal parts) or pastes (Lassar's paste without salicylic acid) are first prescribed, and to reduce itching, 5-10% thymol, thiolum, or naphthalan can be added to the prescribed powder, lotion, or paste. In the weeping stage, it is better to avoid such prescriptions and treat by the 'wet method,' i.e., prescribe compresses (e.g., Burrow's solution diluted with 8 parts water, 1/2-1% borax solution, 7½% alzol solution), which are applied frequently during the day (without allowing them to dry), and at night—an indifferent ointment (e.g., 1% boric, or: Rp. Boracis 0.5, Ung. emoll., Lanolini aa 15.0, Glycerini 3.0), to which one of the above-mentioned anti-itch remedies can also be added. This treatment is carried out for 5-7 consecutive days until the weeping stops. Subsequently, ointments are prescribed, starting with milder (indifferent) ones and gradually progressing to stronger ones containing various anti-eczema remedies (sulfur, resorcin, tar preparations, etc.). Example prescriptions: Rp. Naphthalani 1.5-3.0, Ung. Cetacei, Lanolini aa 15.0. MDS Ointment.—Rp. Resorcini puri 0.3-1.0, Ung. emoll. 30.0. MDS Ointment.—Rp. Sulfuris pp. 01. Fagi (Rusci) 53, 1.5-3.0, Ung. Cetacei, Lanolini aa 15.0. MDS Ointment.—Rp. Sulfur, pp. 1.0-3.0-5.0, Ung. Cetacei, Lanolini aa 15.0. MDS Ointment.—Rp. Sulfidali 1.0-3.0, Ung. cerei 30.0. MDS Ointment.—Rp. Sulfur, pp., Liq. carb. det. aa 2.0, Ung. Cetacei, Lanolini aa 15.0. MDS Ointment. It is better to avoid prescribing vaseline as a base for ointment if the vaseline is not of impeccable quality, since insufficiently purified vaseline has an irritating effect. Pastes with various anti-eczema remedies can also be used. In cases prone to exacerbations, oil suspensions can be prescribed instead of ointments (e.g., Linimentum calcareum or: Rp. Zinci oxydati 60.0, Olivar. 40.0. MDS). In chronic E., stronger concentrations of ointments are prescribed, and ointments with pyrogallic acid or chrysarobin (1-2% and up to 5%) are also used. It is useful to take local hot baths before bed with a solution of potassium permanganate or a decoction of oak bark or chamomile. Specific therapy for E., depending on the location and nature of the inflammatory phenomena, requires an individual approach. In lesions of the hairy part of the scalp, usually with the formation of crusts that glue the hairs together, it is first necessary to remove the crusts by moistening (and possibly applying a compress dressing) with some vegetable oil to soften them. Sometimes it is necessary to cut the hair. The skin of the hairy part of the scalp is generally less irritable, so there is no need to fear washing with water and soap. After the crusts are removed, treatment is carried out according to general rules, and it is better to avoid pastes, lotions, and powders and use compresses or soft ointments. In dry forms, the prescription of various alcohol solutions [Rp. Liq. carb. deterg. 5.0, Ol. Ricini 1.0, Spiritus vini (75%) 100.0, MDS] for wiping the skin is appropriate. In lesions of facial skin, treatment should be carried out with caution due to the excessive irritability of the skin. The same should be kept in mind for E. of the nipples. E. in skin folds and on adjacent skin surfaces (under the breasts, area of the inguino-genital surfaces) requires the application of dressings that separate the adjacent surfaces. In the anal area, lotions or pastes are preferred, and sometimes suppositories have to be prescribed. On the extremities, treatment is carried out according to general rules, and often in lesions of the hands and feet, large blisters have to be punctured; in chronic forms, hot local baths are prescribed. In hyperkeratotic forms, ointments with salicylic acid and compress dressings are prescribed. In persistent weeping forms, the application of 1-2% silver nitrate solution is sometimes helpful. In persistent chronic forms, especially lichenified and infiltrated E., it is often necessary to resort to radiotherapy. Light treatment for eczema is carried out according to the indications of the particular case. General sun-air baths or general irradiation with mountain sun have a beneficial effect on E. in anemic and scrofulous individuals. In acute inflammatory phenomena, the local application of red light helps reduce itching and inflammatory phenomena. In chronic limited eczematous foci, a Kromayer lamp may be used. But generally, the therapeutic value of ultraviolet rays for E. is small, except for seborrheic E. X-ray or Buchi rays (borderline rays) work better and are widely used in chronic forms of E. (acute E. is not suitable for such treatment). X-ray rays are used in fractional doses (^g/₃ HED) in 2-3 sessions with intervals of 1-2 weeks. After the first session, an exacerbation of the process is sometimes observed, but as a rule, itching disappears very quickly, and subsequently the eczematous process undergoes regression. The effect is particularly good in chronic lichenified or infiltrated E., which is usually resistant to drug therapy. Recurrences are possible after radiotherapy; repeated treatment with X-ray rays should be done with caution and after a long interval (6 months or more). During radiotherapy, local drug therapy is discontinued, and especially care must be taken to avoid preparations containing salts of heavy metals (bismuth, mercury, zinc). Buchi rays are also given in fractional doses (150-300 g) with intervals of 8-10-15 days. Buchi rays have an advantage over X-ray rays in that with them, especially during repeated treatment cycles, there is no need to fear late side effects as with X-ray rays (skin atrophy). The disadvantage of Buchi rays is the limited field of action (maximum 10 cm in diameter) and the often observed rather prolonged excessive pigmentation of the skin. In cases of widespread chronic E., some authors recommend indirect radiotherapy—by illuminating the spinal area to affect the intervertebral sympathetic nodes (2 areas in the thoracic and 2 in the lumbar part at ^x/₃ HED with 0.5-mm zinc and 1-mm aluminum filters with the tube tilted at 45° on both sides), repeating the sessions 2-3 times with two-week intervals. Furthermore, for the treatment of E., treatment with radium and radon emanation or Thorium X in the form of freshly prepared ointments or solutions has been proposed. The results are similar to radiotherapy. Seborrheic eczema (eczema seborrhoicum) presents a distinctive picture of a skin disease; first identified by Upp in 1887 as a parasitic E., characterized by round or polycyclic outlines of skin lesion foci (syn.: seborrheite Brocq, eczematide Darier) [see separate table (vol. XXXIV, pp. 635-636), fig. 5]. The symptomatology of seborrheic E. consists of a tendency to primarily affect the hairy part of the scalp, spreading downward from the face (area of eyelids, folds of the wings of the nose, nasolabial, retroauricular, ear canal, chin area), lateral surfaces of the neck, area of the sternum, supra- and infraclavicular spaces, area of the navel, inguinal folds, area of the genital organs, axillary pits, elbow bends, on the back in the area of the shoulder blades and along the spinal column to the sacrum, anterior-internal surfaces of the thighs, popliteal pits, backs of the hands and feet. This preferential location is probably due to the excessive supply of skin fat in these areas, although foci can also be located in other places and in particular on the palms and soles, which lack sebaceous glands. Essentially, seborrheic E. is not connected with increased skin secretion, which is merely a concomitant of E., but rather with excessive formation of autochthonous epidermal fat, which differs from the fat of the sebaceous glands. The morphological elements of seborrheic E. are spots or nodules of yellowish or yellowish-red color of various shades—from the color of normal skin to brown, and the initial elements have a tendency to increase in size and merge with each other, forming outlines of various shapes, usually tending to serpiginous growth.

The surface of the foci is usually covered with small greasy scales; it has a matte tint, unlike the oily seborrhea, and does not tend to weep (the latter may appear when the foci are irritated by pus or irritating chemical substances). The following varieties of seborrheic E. are distinguished: 1) ecz. seborrh. papulatum (Unna) - the presence of yellowish, scaly papules or spots; 2) ecz. seborrh. circuit scriptum - with sharply defined borders; ecz. seborrh. nummulare - in round coin-like disks; ecz. seborrh. annulare - in ring-shaped outlines; ecz. seborrh. petaloides - in the form of a palm leaf along the spine with branches in the intercostal spaces; 3) ecz. seborrh. magnareatum flavum, fuscum - in large foci; 4) ecz. seborrh. psoriasiforme - in sharply scaling foci; 5) ecz. seborrh. exfoliens universalis - in the general scaling form; 6) ecz. seborrh. pityroides - in dry bran-like scaling; 7) ecz. seborrh. erythemato-pityroides - in clearly expressed redness and scaling, etc. Subjective disturbances are either absent or patients note itching, which intensifies at night or during sweating. The course varies in different cases: sometimes the process remains stationary on individual foci for years, improving in summer and worsening in winter; sometimes it tends to give flare-ups of spread or to undergo regression. The so-called dry seborrhea of the hairy part of the scalp is considered by some as the initial form of seborrheic eczema. The etiology of seborrheic E. remains unclear: its parasitic nature is rejected, since the role of any microorganisms in it, including Unna's 'micrococci', could not be proven by anyone. In some cases, the occurrence of E. can be linked with gastrointestinal abnormalities (constipation, chronic colitis, etc.), metabolic disorders, disorders of the endocrine system, etc. Diagnosis is based on the clinical picture, the nature of spread from top to bottom, and favorite localization; differential diagnosis with other dermatoses (psoriasis vulgaris, pityriasis rosea, lupus erythematosus, etc.) is easily carried out. Treatment of seborrheic E. is conducted on the same principles as the treatment of banal E., i.e., general (depending on the presumed general disease predisposing to the occurrence of E.) and local treatment of the inflammatory process, with the latter being conducted with more energetic preparations, since seborrheic E. is less prone to exacerbations. In acute manifestations, treatment is conducted according to the stated principles for acute banal E. Otherwise, various preparations are used, such as sulfur, tar, resorcin, salicylic acid, pyrogallol, chrysarobin, etc., in the form of ointments, mixtures, pastes, solutions, for example: Rp. Sulfur, pp. 3.0, Resorcini puri 0.5-1.0, Ung. Ceteacei, Lanolini aa 15.0. MDS Ointment.-Rp. Sulfur, depur., Resorcini, Ichthyoli aa 2.0, Ac. salicyl. 1.0, Vaselini ad 50.0. MDS Ointment.- Rp. Chrysarobini, Ichthyoli aa. 5.0, Ac. salicyl. 2.0, Vaselini ad 100.0. MDS Ointment.-Rp. Sulfur. pp. 12.0, Camphor, tr. 1.0, Muc. Gummi arab. 6.0, Aq. rosarum, Aq. Calcis aa 100.0. MDS External.-Rp. Sulfur, pp., Kal. sulfur. aa 10.0, Zinci sulfur. 4.0, Aq. Rosae ad 100.0. MDS External (Lotio alba).-Rp. Sulfur, pp. 4.0, Zinci oxyd. 6.0. Terr. silic. 2.0, Axung. benz. ad 50.0. MDS Paste.-Rp. Sulfur, pp. 5.0, Ac. salicyl., Resorcini aa 1.5-2.5, Vaselini ad 50.0. MDS Ointment.-Rp. Resorcini, Ac. salicyl. aa 1.0, Ol. Rusci 5.0, Sap. med. q. s. ad emuls., Sulfur, pp. 5.0, Axung. benz. ad 50.0. MDS Ointment.-Rp. Pyrogalloli, Ichthyoli aa 5.0, Ac. salicyl. 2.0, Vaselini ad. 100.0.- Rp. Tumenol-amm. 8.0, Anthrarobini 2.0, Tinct. Benzoes 30.0, Aether, sulf. 20.0. MDS Smearing.-Rp. Ichthyol-amm. 3.0, Boli rubr. 0.5, Boli alb. 2.5, Magnes. carb. 4.0, Zinci oxyd. 5.0, Amyli Oryzae 8.0. MDS Powder.- Rp. Sulfur, pp., Ol. Fici aa 1.5-3.0, Pasta Zinci 30.0. MDS External.-For hairy parts of the scalp, ointments or alcoholic solutions are preferred. In widespread foci and in cases prone to worsening in winter, general irradiations with mountain sun are prescribed, and in summer, general sun-air baths are given to such patients. X-ray therapy is used in stubborn cases of limited foci. Treatment with boundary rays gives satisfactory results.

M. Demyanovich. Eczema in childhood. E. occurs mainly in young children - in approximately 4% of children attending consultations (Sokolov, Warsaw). It sometimes appears very early - in the first weeks of the child's life, but more often not before 3-4 months of age, and persists, improving and then exacerbating again, very stubbornly until 2-4 years of age, in some cases longer, and sometimes in one form or another throughout life. The favorite locations are the face and the hairy part of the head; on the face, E. most commonly affects the cheeks, chin, forehead, and the skin folds behind the ears, leaving the skin around the mouth free. On the cheeks, it develops from seborrheic dermatitis (Mogo), which has been given the name 'milk crust' (Milchschorf). On the hairy part of the head, the formation of greasy crusts on the weeping surface of E. is very common, as well as its purulent infection, which provides material for more abundant crust formation. Larger or smaller foci of E. also form on other areas of the skin, in some cases foci in the skin folds persist particularly stubbornly, mainly in the popliteal and cubital areas, and on the hands. Persistent intertrigo, as well as Leiner's desquamative erythrodermia, which occur in children in the first weeks of life, are apparently genetically related to E. and sometimes run concurrently with it. E. is not a local disease; it is the result of abnormalities in the metabolism of the entire organism and arises in the child always on a constitutionally pathological basis: most often it is an exudative diathesis, or one very close to it, arthritism, or a lymphatic-hypoplastic constitution, and sometimes another congenitally inadequate basis, for example, the eczema of Mongoloids and others. In some cases, such a basis is created by congenital syphilis. The opinion that tuberculosis plays an etiological role in E. is not proven by anything and seems unlikely. The constitutionally inadequate basis is characterized, among other things, by the history of exudative individuals: frequent thyroid gland lesions in parents (33% of cases), diabetes (18.5% of cases), further gout, epilepsy, etc., as well as morphological signs of developmental delay (Sokolov). The general condition for the development of E. on this basis is apparently an allergic state; in children or their families, various manifestations of allergy can often be noted: bronchial asthma, urticaria, Quincke's edema, etc. In addition, this is indicated by the increased eosinophilia in the blood and tissues of eczematous individuals, positive skin tests with various proteins, the Prausnitz-Küstner phenomenon, and many others. The appearance of E., or its exacerbation, is mainly connected with moments of an alimentary nature (the beginning of supplementary feeding with milk, irregular feeding, etc.) or infection, for example, influenza, vaccination; however, it is no less common in children on purely breast milk and without a clear cause. Sometimes, disappearing with age, E. leaves its equivalent - bronchial asthma, prurigo, Quincke's edema, etc. The prognosis, despite the duration and stubbornness of the disease, is good; E. rarely gives severe complications threatening life. Among these should be mentioned: nephritis, probably caused by streptococcal infection of E., and sepsis from the same cause. Occasionally, sudden death in E. (Ekzemtod) is observed, which is associated with status thymico-lymphaticus (Paltauf, Hedinger), as well as with absorption from the surface of the eczema. Prevention of E. in children predisposed to it consists in establishing proper feeding of the child, avoiding violations of routine, infection, constipation and diarrhea. In such children, early supplementary feeding with milk should not be started; milk should generally be limited. When E. has already appeared, diet treatment comes to the forefront. Americans proposed regulating the diet of the child (and his mother) on the basis of skin tests, discarding everything to which the child reacts positively; in practice this does not give reliable results. With breastfeeding, careful restriction of the mother's milk, early supplementary feeding (not with milk), and transfer to another woman's breast are recommended. In a child on mixed and artificial feeding, cow's milk should be limited and food that reduces the manifestations of E. should be sought by temporarily excluding one or another component of the diet while observing the course of E. Sometimes replacing cow's milk with goat's milk has an effect. However, diet therapy often does not give reliable results, and E. heals on a full diet. The child should not be kept for long on a hungry and one-sided diet; from this point of view, Finkelstein's eczema soup is a risk. General drug treatment is often used - sulfur and calomel (Lesage) in minimal doses, Thyreoidin (the French), CaCl2 in a 5% solution. Antitoxin and hemotherapy do not give any appreciable results, nor does CaCl2 into the vein; Peguy and Oulagnier (and Thu, Aulagnier) recommend an enterococcal vaccine. A somewhat greater effect is obtained in some cases from the quartz lamp, and especially from the so-called Bucky rays. Local drug treatment - according to general rules.