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VESCICLES. II.Atopic Dermatitis.Diagnosis. Diagnosis of atopic dermatitis (AD) is easy when this disorder involves for a long period, with a seasonal chronic-fluctuating course, the classical sites, notably the elbow and knee flexures. Diagnosis can be difficult during the first three months of life and in the presence of lesions complicated by other factors or characterized by an atypical morphology and distribution, i. e. asymmetrical (Fig. 500).
There is no single clinical sign or a biological alteration which is always detected in AD. Therefore, the diagnosis of AD is based on the contemporary presence of some diagnostic criteria, the most well-known of which were proposed by Hanifin and Rajka. They include:
According to these Authors, at least two of the above-mentioned criteria must be satisfied for diagnosing AD. This is not applied for children before the age of three months in whom two of the above criteria are generally not satisfied (Tab. 2). Tab. 2 1- Eczematous lesions of the face and/or scalp with minor or no involvement of the diaper area. 2a- First-degree relative with atopic dermatitis and/or allergic/rhinitis. 2b- Restlessness and/or sleeplessness non attributable to other causas. To diagnose atopic dermatitis in the first three months, the criterion 1 must be satisfied and associated with the criterion 2a and/or 2b. The chronic fluctuating course cannot be appreciated at this age and also the scratching reflex, which is not completely developed before this age. Furthermore, a personal history of other atopic disorders is not present during the early months of life as AD is generally the first manifestation of the atopic constitution. On the basis of these considerations, we suggest that the major diagnostic criterion during the first three months of life is represented by the occurrence on the face and scalp of eczematous lesions with mild or no involvement of the diaper area. We have also proposed that at least one of the following minor criteria should be associated with the above-mentioned major criterion: a- a close relative affected by allergic asthma-rhinitis or atopic dermatitis; b- restlessness and/or sleep-lessness unrelated to other factors. Differential diagnosis. AD must be distinguished from neonatal acne, seborrheic dermatitis presenting as cradle cap, constitutional keratosis rubra and the other itching dermatoses of childhood, in particular scabies. Neonatal acne. It is also called hormonal crisis of the neonate. Neonatal acne and seborrheic dermatitis are the more frequent differential diagnoses in the first two months af age. Although lesions of neonatal acne are symmetrically distributed on the cheeks, morphologically they consist of comedo papules or follicular pustules (Fig. 501, 503), which are grouped but not confluent. They are not associated with psychomotor agitation and run a characteristic clinical course, starting before the end of the third week of life, therefore more precocious than AD and spontaneously clearing up by the age of six weeks, when AD usually starts. In its initial phase AD can be characterized by isolated papules and vesicles (Fig. 502). However, in a few days the lesions get confluent giving raise to more or less exudative, erythematous, scaling and crusted patches (Fig. 504). "Cradle cap" seborrheic dermatitis. This disorder is poorly defined from a clinical point of view. This is why several Authors do not consider seborrheic dermatitis as a separate entity. As a matter of fact, it is not possible to include in the heading of seborrheic dermatitis disorders of very different frequency and severity, ranging from the frequent and mild "cradle cap" to the severe, sometimes lethal Leiner’s erythroderma, which is due to a primary immunodeficiency. A mild desquamation of the scalp and glabella is reported in most children before the age of three months and these patients are generally not referred to the dermatologist. These cases are generally considered "cradle cap". This very frequent disorder, which spontaneously regresses within a few weeks, is not probably related to AD. When desquamation involves more than 30% of the scalp (Fig 505, 507) or is associated with exudation (Fig. 506, 507), psychomotor agitation or other cutaneous lesions besides the glabella, we are probably dealing with an initial AD and not with a case of "cradle cap". Psoriasis-like dermatitis. Some Authors still include this disorder in the heading of seborrheic dermatitis. On the other hand, it is an expression of psoriatic constitution, as indicated by its name. The children who suffered from psoriasis-like dermatitis, develop sometimes a classical form of psoriasis later on. The percentage of these children is 5% after a 10-year follow-up and increases with time. The dermatitis typically starts with lesions involving the diaper area. After a few days or weeks it involves with punctate eruptive manifestations all the cutaneous surface. It differs from AD (Fig. 509) for the constant and prevalent involvement of the diaper area (Fig. 508), the morphology of the lesions, which are characterized by well delimitated edges and centrifugal evolution, and, finally, the spontaneous and definitive resolution of the eruption within 4 - 8 weeks. On the other hand, the dermatitis involving the diaper area, can persist for weeks or months or regresses only when the diaper is withdrawn. Constitutional keratosis rubra is characterized by a symmetrical rubeosis of the face with a follicular keratosis which may simulate AD (Fig. 510). This condition is genetically determined and tends to improve with time (decades). It is not associated with itching, desquamation, or other types of cutaneous lesions. Ischemic areas are alternated with areas of vasodilatation (Fig. 511). It begins predominantly at the end of the first year of life when the lesions of AD situated on the cheeks tend to disappear. Among the itching dermatoses of childhood, scabies must be more often distinguished from AD. Scabies (Fig. 512) is a contagious disorder and may affect contemporarily several members of the same family. The onset of scabies is more acute and the classical sites involved with AD, especially the face, are generally spared. Scabies is predominantly localized on the ulnar aspect of the hand and the anterior axillary pillar (Fig. 512). Gross nodular lesions, polymorphous lesions, notably vesicles, papules, pustules and nodules, and sometimes the pathognomonic burrows may also be characteristically observed. However, burrows can be hardly visible in most cases. Laboratory investigations. Routine laboratory investigations, dosage of total and specific IgE and analysis of mast-cells associated IgE antibodies are invariably performed in children with AD. We have made these investigations for over 15 years and at the beginning of the nineties, we wondered if it was still worth performing these tests. Dosage of total serum IgE has little value in the diagnostic procedures of AD as they have a wide range of variation in the normal individual and moreover are not elevated in more than 30% of subjects with AD. Furthermore, they may be increased in several other conditions including the most frequent itching dermatoses of childhood, notably scabies, insect bites and dermatitis herpetiformis. Dosage of IgE directed against environmental allergens is more useful but quite difficult to evaluate. It is useful as the atopic subject shows IgE antibodies directed against several environmental substances. This finding may confirm the diagnosis of AD in uncertain cases. However, it is difficult to be evaluated as parents request this test to determine the cause of AD and not to confirm the diagnosis of AD, which is easily recognized. However, several experts suggest that the demonstration of IgE antibodies specific for environmental substances does not indicate an obligatory involvement of these substances in the development of the clinical manifestations of AD. Skin tests performed for demonstrating IgE antibodies associated with mastocytes have the same clinical significance of the dosage of serum IgE antibodies. In the recent years, patch tests with evaluation after 48-72 hours became popular. These tests can detect a positivity for chemical compounds and thus show an allergic contact dermatitis complicating AD. Furthermore, patch tests can also detect a positivity for the same allergens (pollens, foods), which are tested with prick tests. The clinical significance of these delayed reactions, however, has not been yet fully elucidated. Double-blind, placebo-controlled challenge tests may indicate a possible role of a specific substance in AD, though they cannot clarify if the pathogenesis is determined by an allergic mechanism or not. Prognosis. How long may AD last? We can respond to this questions in two ways as follows: the condition may clear in a few months or years, or alternatively, may persist for life. In fact, although the common infantile phase is observed from 6 months to the age of 2 years, these subjects show an atopic constitution throughout their life and therefore may develop at any time exaggerate cutaneous reaction to agents or situations which are normally well tolerated by the skin of normal individuals. However, the first answer is the most appropriate as it reassures the often anxious mothers that the dermatosis affecting their child will disappear after a few months or years. It is impossible to indicate to the mother the exact duration of AD in her own child. How-ever, statistical analyses have shown that most cases of AD initiating after few months of life improve consistently after the first summer, unless during this season the child is aged 6-7 months. After a few years, the number of children with AD tend to progressively decrease and become irrelevant by the age of 6. In our opinion, neither a clinical sign nor a laboratory finding may indicate the exact duration of AD. We can only very simply say that longer the duration of AD, worse its prognosis. AD beginning after few months of life and still present at the age of 6 years will probably last for several years. For this reason, prognosis and therapy of cases of AD with the same clinical picture will vary according to the duration of the disease. Consequently, the management of a case persisting for six months will be different from that of a case which has been present for six years, even though both cases are characterized by the same extension and severity. Therapy of infantile AD. Therapy of AD is difficult and frustrating for both parents and physicians. Difficulties are similar to that encountered in the treatments of all the chronic diseases scarcely responding to treatments. Furthermore, AD is frequently and easily recognized by physicians with different clinical backgrounds who do not have the same opinions on the treatment of this condition. This confirms the lack of a unique view on this disorder and this is the cause of anxiety in the family. AD is characterized, as well as many other skin diseases, by a very variable severity. This is why, in our pinion, AD needs a gradual therapeutical approach. A- Erythematous AD. It is not exudative and involves less than 5% of the skin surface. Minimal infantile AD of the face and minimal relapsing AD of the elbow and knee flexures affecting the child aged 3-6 years are included in this form. When the diagnosis of AD is made, it is necessary to inform the parents on the significance of the disease (familial predisposition, association with other atopic disorders, natural history of the disease). In several cases, the mother is very anxious and it is therefore necessary to discuss with her to explain that AD is a benign condition. In particular, the physician should inform the mother that AD is the most frequent dermatitis of childhood, is not contagious, does not leave scars, and, moreover, will disappear within a few years. It is also important to reassure the mother that in this case AD affecting her child is not a severe form as only localized areas are involved and, furthermore, epidermal alterations and exudation, which may exacerbate the disease, are not present. After this preliminary approach, the appropriate therapy should be established. The clinical history may demonstrate factors exacerbating the disease (please see Eur. J. Pediat. Dermatol. vol. 6, pag. 228) which should possibly be eliminated. In the absence of significative anamnestic data, it is not recommended in these minimal forms to perform tests for specific IgE antibodies. A symptomatic therapy will be then prescribed. In these minimal forms, I tend to avoid pharmacologic treatments, in particular if itching does not affect the vegetative and social life of the child (Fig. 513, 514). I also discuss with the mother about the possible symptomatic therapies and their scarce effect on these minimal forms. I explain that it is difficult to predict and prevent a possible future exacerbation of the disease as we are not dealing with a disorder caused by a single exogenous factor which can be easily identified and eliminated, such as an infectious agent. I also recommend to observe carefully and without prejudice the response of the child to the most common irritants (tomato, Parmesan cheese, rough clothes made by wool or synthetic fibres) and to avoid these irritants only if a clear intolerance is demonstrated (for example, the mother should not always eliminate tomatoes, but must use a small spoon to feed the child avoiding to dirty his/her mouth and hands. She also should clean the child with lukewarm water and dry the skin without rubbing it. In particular during the first year of life, I recall to the mother that although her child is not contagious, he can be more easily affected by some infectious diseases, notably primary herpes simplex infection. Therefore he should not be kissed by relatives with a recidive of labial herpes simplex. B- "Cradle cap-like" AD. This form is frequent during the first 6 months of life. When the hair is quite short and the squamo-crusts are very thick (Fig. 507), the treatment with a petrolatum-based cream for a few hours can be useful. If the hair is longer and the scales are not thick, the cream can be hardly removed and therefore the utilization of petrolatum oil for a few minutes before the shampoo is more indicated. The squamo-crusts must be manually removed as they do not detach spontaneously. After the asportation of the squamo-crusts, a corticosteroid cream must be applied on the irritated or exudative skin. In the presence of long hair, an aqueous corticosteroid lotion (desoxymetasone 0.025%) is indicated. C- Eczema-like AD is characterized by several patches which may not show erythema or may present only a modest erythematous component. They develop a pityriasic desquamation or a follicular keratosis and subside leaving depigmentation. This hypopigmented phase of eczematous AD is more evident at the end of summer and in autumn and is generally not itching. This minimal form of AD may involve the face ("pityriasis alba faciei" -Fig. 515-), the limbs and rarely the trunk (Fig. 516). In spring time this minimal phlogosis is represented by well delimitated red patches with fine scaling or follicular hyperkeratosis which are respectively responsible of skin roughness or rasp-like skin. In summer time, the minimal phlogosis involving both the superficial dermis and the epidermis affect the traffic of the melanocytic pigment from the basal melanocytes to keratinocytes. Consequently, at the end of summer there may be the appearance of white patches which reproduce the form and dimensions of the pre-existing rough lesions and are often esthetically disturbing. On the other hand, at this time the rough and rasp-like skin is no more visible. For these white lesions, the child is generally referred to a physician. Unfortunately, many times these patches are erroneously treated for a long period of time with antimycotic creams because they are misdiagnosed as cutaneous mycosis, notably pityriasis versicolor, which is the most frequent superficial mycosis. However, pityriasis versicolor cannot be observed in childhood as its etiologic agent needs the presence of the superficial sebum which is produced under hormonal stimulation only after puberty. The natural history of pityriasis alba is characterized by a slow and spontaneous regression within about 6 months. The regression is due to the loss of tan of the normal skin surrounding the hypochromic patches and not to the reacquisition of melanin. Physicians should also be aware and inform mothers that this form of AD may relapse for several years. From a therapeutical point of view, the approach is similar to that of form A- minimal erythematous AD and therefore it is also not useful to perform tests for specific IgE. With regard to the symptomatic therapy, it is necessary to stress that only with time will the skin return to a uniform color and there are no therapies which may improve the esthetic situation of the hypochromic phase. In the spring phase of minimal phlogosis with desquamative patches or follicular hyperkeratosis, a therapy is not required for the child who has no itching and is not disturbed by the roughness of his/her skin surface. Furthermore, infective complications are not observed in this form as the hyperkeratotic skin is thicker and thus more resistant and, moreover, scratching is not present. Consequently, it is only the mother that may request for esthetical reasons a treatment as the child does not present a subjective symptomatology and prevention of infection is unnecessary. Therefore, after carefully explaining to the mother the natural history of these lesions, we must suggest to avoid the treatment of this condition, in particular during the autumnal hypopigmented phase. During the desquamative or hyperkeratotic phase a treatment is indicated only in the presence of evident and extensive lesions. In the presence of evident lesions, an emollient cream can be prescribed. Hundreds of emollient creams are commercially available and their census is becoming more and more difficult. Furthermore, their expensive price -from two to six times more than a steroid cream- as well as the insistent advertising recommending their use rises some doubts on their real therapeutic significance. These creams are mainly requested by the mother of the child. In fact, since she generally applies these creams on her face, she believes that the skin of the child has similar problems and needs the same treatments. After explaining to the mother that the skin dryness of his child is caused by the minimal phlogosis of the skin induced by AD, a cream will be prescribed provided that it does not cause cutaneous redness, which is a frequent complication. Furthermore, the application of this cream must not be the cause of daily fights with her child. Emollient creams containing non-steroid mild antiinflammatories are commercially available. Their good performance is consistent with the view that the dryness of the atopic subjects is due to a minimal phlogosis. However, a mild steroid cream diluted (1:5 or 1:10) with a common emollient cream produces the same effect and is much less expensive. Before recommending this approach, it is necessary to reassure the mother that the prejudicial fear against the corticosteroid therapy is not justified. However, this matter will be discussed later on. In the presence of extensive lesions an emollient bath should be prescribed. The frequency of baths is determined by the wish of the child. He may be bathed daily, or, alternatively, if the bath represents an unpleasant event for the child, its frequency can be reduced. An emollient bath is an oil or an oil-water emulsion which is used in place of the soap. It is useful massaging with the emollient the skin of the child immersed in the water in order to remove the scales. The simplest emollient, e. i. petrolatum oil, is probably the best. D- Exudative localized AD involving less than 10% of the skin surface. This type includes the classical forms of AD affecting the face (Fig. 517, 518) during the first year of life and the knee and elbow flexures (Fig. 519, 520) from the second year of life onwards. In these forms, although the lesions are not extensive, the individual lesions are quite severe and cause cracking of the skin surface. Also in these forms, a conversation with the parents is necessary. It must be stressed that prevention of infection is indispensable because of the presence of cracking in correspondence of the skin lesions. These forms are characterized by intense itching which responds rather well to the symptomatic treatment. This matter will be discussed in more detail later on. Therapy is necessary for the exudative lesions of the face as all the three conditions indispensable for starting a symptomatic treatment are present. They include itching and its repercussions on the vegetative and social life of the child, risk of infectious complications and esthetic disturbances. Only this last complication is not observed in the exudative lesions of flexures, which therefore also need a symptomatic treatment. When these localized forms of AD respond to the symptomatic treatment, the dosage of specific IgE for environmental allergens is unnecessary. Topical steroid is the symptomatic treatment of choice for the exudative forms. This is the only therapy which has an immediate visible effect in AD. This effect consists in the temporary blockade of exudation and in the diminution of both erythema and itching. Topical steroids must be considered a drastic
treatment and therefore the physician who prescribes this
drug must be aware of its mechanism of action, metabolism
and side-effects. A topical steroid cannot be prescribed
without the consensus of the mother who has often a
prejudicial fear for this medicament, caused by the
numerous reports published by dermatologists between the
seventies and the eighties, in which the several
side-effects of steroids were described. Topical steroid is the drug with the best anti-inflammatory effects. It has a limited ability to penetrate the skin and therefore is particularly indicated in the phlogistic lesions of both the superficial dermis and the epidermis, namely in the eczematous lesions. Its antiinflammatory activity is transitory and disappears rapidly after the suspension of the therapy. This defect of the corticosteroid creams has been emphasized and several mothers have decided to avoid its use because the dermatitis often relapsed after the suspension of the treatment. Topical corticosteroid reduce inflammation, itching and the risk of infections restoring skin integrity and the esthetic aspect of the child. In practice, it improves the quality of life of the child with AD (Fig. 521, 522). However, topical corticosteroids as well other effective drugs do present several side-effects. Among the systemic side-effects observed in the past for their inappropriate use, it must be remembered the iatrogenic Cushing's syndrome (Fig. 525) caused by the topical application of steroids in the diaper area. Several local side-effects have been reported, in particular drug addiction. The first applications have generally a consistent antiinflammatory effect. If the corticosteroid applications are continued, the same antiinflammatory effect can be obtained only with progressively greater doses. Furthermore, the sudden withdrawal of topical corticosteroid therapy after a prolonged use may exacerbate significatively the inflammation. Other local side-effects include thinning of the skin, hypertrichosis and granuloma gluteale infantum. This latter dermatosis is characterized by a pseudo-tumoral appearance (Fig. 527) and subsides leaving atrophic scars. Hypertrichosis and thinning (Fig. 523, 524) of the skin subside if the topical corticosteroids are discontinued. Hypertrichosis (Fig. 526) is the main cause of fear of the mothers: it consists of a transitory thickening of the hair shaft, which makes more visible the vellus hair present throughout all the cutaneous surface with the exception of the palmo-plantar regions. Topical corticosteroid therapy may also induce the development of striae distensae (Fig. 528). These may already be present in physiological situations characterized by an increased concentration of steroid hormones, notably pregnancy and puberty. Striae distensae are generally distributed in correspondence of specific sites, notably roots of thighs, flexures, and hypomesogastric regions. During puberty, the use of topical corticosteroids in these sites is therefore not indicated. A further side effect, which must be recalled to the mothers for avoiding unjustified anxiety, is the sudden development of pallor in correspondence of the inflamed skin after the application of corticosteroid creams. This event is the result of a reactive vasoconstriction induced by the drug. The knowledge of these side effects is essential for avoiding their development. It is also recommended that the topical corticosteroid is prescribed after a discussion which informs the mother about the symptomatic and temporary effect of this medicament. It must also be clarified to the mother that topical steroid is the most valid treatment for the localized forms of AD, when causal treatments are lacking. The mother must also know that topical corticosteroid is a drastic treatment which, however, is not harmful if it is correctly used. Finally, the mother must be clearly informed how much, where and how long the topical corticosteroid must be used. How much. The total amount of topical corticosteroid to be applied in a defined period of time must be clearly specified to the mother avoiding vague definitions, such as "just a bit" or "as less as possible". It is necessary to explain to the mother that for example a tube containing 30 g of a mild topical corticosteroid should last for 20 days. The duration depends on the age, the extension of the cutaneous surface involved by the eczema and the eventual need for obtaining an immediate effect. It is necessary to explain to the mother that if a treatment of 20 days using the amount of corticosteroid cream contained in a tube is prescribed by the dermatologist, it does not mean that one tube should not last less than 20 days and may last six months. On the other hand, the tube must last 20 days and not 10 days or 30 days. It is suggested to tell her the anecdote about the pernickety mother who, being aware that the tube had to last for 20 days, squeezed out the cream contained in the tube on a table forming a straight line. She then measured the length of the straight line with a ruler and divided the cream in 20 parts in order to know the exact amount of cream which had to be used for each application. Obviously, it is necessary to adapt with elasticity the consume of the cream to the duration of the treatment. For example, if after 10 days the tube is finished, this means that too much cream has been utilized. Alternatively, if after the same period of time the tube is almost complete, it is evident that an insufficient amount of cream has been applied. Where. If the dermatitis is extensive, the corticosteroid cream must be not applied on the healthy skin situated in the periphery of the lesions and/or between two lesions. It is also unnecessary to treat areas of skin characterized by a mild erythema. Congestive and exudative lesions with acute phlogosis are instead best treated with a topical steroid cream. In some sites, topical corticosteroid creams must not be applied or must be used with great caution. The diaper area is one of these sites. This area is rarely involved with AD and therefore systemic and local side effects, such as granuloma gluteale infantum, have more often been observed in the past as a complication of the steroid treatment of primary irritant diaper dermatitis (Fig. 525, 527). It is often reported that the face is one of the sites where the use of topical steroids is not recommended as the skin is quite thin. However, we have rarely observed on the face side-effects caused by the use of topical steroids, except in rare cases of transitory hypertrichosis (Fig. 526). Mild topical steroids can be used on the upper eyelids, which are frequently affected by eczematous lesions. We have also rarely observed striae distensae (Fig. 528) in correspondence to the popliteal flexures determined by the application of topical steroids during the prepuberal period. However, during this period it is not recommended to use steroid creams in the popliteal flexures and the other sites preferentially affected by the striae distensae. How long. The effect of a valid steroid is immediate, though it tends to become less efficient as the time passes. For this reason, the topical steroid must be used until the disappearance of both exudation and intense erythema. This may happen after the first application or after 2-4 applications. If after 5 - 6 applications the phlogosis is still present, it is useless continuing the utilization of the same topical steroid. Several reasons may be responsible for the lack of response to the treatment. They include in order of frequency: an insufficient application of cream for prejudicial fear, the presence of an infectious complication, intense scratching, an immediate or delayed allergy to environmental substances or cream components. In the latter event, investigations to determine an immediate or delayed allergic mechanism (prick tests and patch tests respectively) are indicated. If the phlogosis has been eliminated, it is unnecessary and harmful continuing the application of a topical steroid. In this case, it is recommended to suspend the treatment and wait for the eventual acute relapse of the phlogosis which must not be considered a therapeutic failure. This must be clearly explained to the mother. In mild cases, a course of topical steroid treatment may induce a definitive remission of the disease. In the majority of cases, the phlogosis returns 4 - 10 days after the suspension of the topical steroid (2 - 3 days in severe cases). If the dermatitis relapses acutely after 1 day, the dermatologist must exclude that this is caused by some of the following reasons, notably an insufficient application of cream, intense scratching, an immediate or delayed allergy to environmental substances or cream components. In the latter event, an investigation to determine an immediate (prick tests) or contact (patch tests) allergy is recommended. Number of applications. A daily application of the most recent steroid creams of medium power is sufficient. The cream can be utilized at any time during the day, also when the child is sleeping if during the day he does not allow the application of the cream. Type of steroid. It is not important. Clobeta-sone-based creams are necessary only when for particular reasons it is desirable an immediate effect in a short period of time. Generally, a corticosteroid cream of medium power once a day is sufficient. Type of vehicle. A water-oil evanescent cream is indicated as the lesions are generally exudative. In the presence of exudative lesions on the scalp, the cream makes the hair dirty. In these case, a lotion is not indicated as it contains alcohol which causes an intense burning. In the presence of hair of normal length, it is therefore indicated the utilization of an aqueous solution of dexossimetazone 0,025%. However, exudative lesions in correspondence of the scalp are generally observed in children between 3 and 9 months of age when hairs are very short and therefore creams can be utilized. Other therapies. Antihistamines are generally not indicated in the localized exudative forms as the intense itching often observed in these forms responds better to topical corticosteroid treatments than to oral antihistamines. For the same reason the antihistaminic treatment must not be administered together with the topical steroid, at least in the first prescription. A sedative antihistamine can be useful only in those cases refractory to the topical corticosteroid treatment or when the role of intense scratching is predominant. Before discussing the therapy of the other forms of AD, it must be remembered that these first four clinical pictures represent about 90% of all AD cases. In these cases neither investigations to find specific IgE for environmental substances nor other laboratory tests are indicated in the absence of specific manifestations, suggesting the occurrence of a complication. Fig. 501: Neonatal acne is characterized by comedo papules and follicular pustules, close each other and non confluent. Fig. 502: Initially, atopic dermatitis can be characterized by monomorphic, isolated papules and vesicles, which then tend to get confluent. Fig. 503, 504: At the age of 3 weeks this baby presented neonatal acne (Fig. 503), which lasted till the sixth week. At the age of 4 months the same baby presented a classical atopic dermatitis (Fig. 504) of the face. Notice the difference in the same site between the isolated comedo lesions (Fig. 503) and the confluent patches of atopic dermatitis (Fig. 504). Fig. 505, 506, 507: When scaling affects large areas of the scalp (Fig. 505, 507) or is associated with erythematous and exudative lesions of the face (Fig. 506) or of the scalp itself (Fig. 507), the diagnosis of atopic dermatitis is certain. Fig. 508: In atopic dermatitis, even very widespread, the classical sites, namely the face in the first year of age, are more intensely affected, whereas the diaper area is scarcely involved. Usually, the borders of the lesions are not well defined. Fig. 509: "Napkin psoriasis" starts in the diaper area. In this area the lesions are usually more erythematous and confluent. Later on, others sites such as the trunk are affected by eruptive lesions with clear-cut borders and tendency to spread centrifugally. Fig. 510, 511: Constitutional keratosis rubra may be reminiscent of atopic dermatitis (Fig. 510). However, it is not itchy. Moreover, follicular papules can be seen (Fig. 511) at a closer view and palpated. Ischemic areas (Fig. 511) can be seen inside the erythematous areas. Keratosis rubra usually starts around the end of the first year, when atopic dermatitis tends to leave the cheeks, and persists for decades. Fig. 512: Usually scabies spares the head and affects the anterior axillary pillars. Moreover, scabies in childhood is characterized by various lesions, included gross nodules. Fig. 513: Erythematous atopic dermatitis. There are no symptoms neither scratch marks. Fig. 514: Erythematous atopic dermatitis. The epidermis is not affected and thus there is no risk of infection. Fig. 515: Eczema-like atopic dermatitis ("pityriasis alba faciei"). The hypopigmented lesions usually relapse for years. Fig. 516: Eczema-like, hypopigmented atopic dermatitis, with minimal eczematous lesions in classical sites, notably face and elbow flexures. Fig. 517, 518, 519, 520: Topical antiinflammatory steroid creams are the treatment of choice for localized exudation, namely for cracking of the epidermis in a limited area -less than 10% of the skin surface- of the face in the first year of age (Fig. 517, 518) and later on of the flexures (Fig. 519, 520). This treatment restores, although temporarily, the skin integrity and reduces itching more than antihistamines. Fig. 521, 522: An 11-year-old girl with atopic dermatitis of the face. The persistence of the dermatitis is also due to a prejudicial fear of topical steroids. After a few days of topical steroid treatment (Fig. 522) the patient can return to a normal relation life (courtesy of Dr. M. Cutrone). Fig. 523, 524: Thinning, usually transitory of the skin, is a side-effect of corticosteroids, even topically applied. The girl as in Fig. 523, with alopecia areata, presents thinned skin, which better puts in evidence the dermal vessels. The thinning of the skin, due to topical steroid treatment, regressed 6 months later (Fig. 524), with total regrowth of the hair. Fig. 525: Iatrogenic Cushing syndrome due to percutaneous absorption of steroids used in diaper rash. Fig. 526: Transitory hypertrichosis due to topical steroids used in atopic dermatitis of the face. Fig. 527: Tumor-like granuloma gluteale infantum due to topical steroids used in diaper rash. Fig. 528: Striae rubrae of the popliteal flexures due to topical steroids used in peripuberal atopic dermatitis.
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