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Common Dermatologic Conditions Seen By the Pediatric Allergist
Common Dermatologic Conditions Seen By the Pediatric Allergist BERNARD A. BERMAN, M.D.iII
The allergic dermatoses, comprising a lengthy list of skin disorders commonly encountered in the day-to-day practice of medicine, present a distinct and singular challenge to the physician involved with their diagnosis and subsequent management (Table 1). Of all these derTable 1.
Allergic Dermatoses (Cutaneous Allergic Reactions)
Eczematoid dermatoses Urticaria Drug eruptions Physical allergy Allergic purpura Reactions associated with acute or chronic infection Reactions associated with autoimmune or collagen disorders
matoses, the most prevalent ones, which bother the physician the most, are the eczematoid dermatoses, commonly referred to simply as "eczema." It can be said of eczema that it is a stubborn skin eruption, characterized by erythema, scaling, oozing, lichenification, or any combination of these, and occurring in subacute, acute, or chronic forms. The eczematoid dermatoses, in effect, constitute a group of skin disorders with some, but not all, features in common. It is not possible in this article to discuss all these disorders fully and completely, and the reader is referred to standard texts. We will highlight a few of the more common and troublesome ones. Our classification (Table 2) is accurate enough in descriptive terms for the classic types, but it ignores the many etiologic components that are present in each case. It does not consider the fact that there is no completely defined pathologic difference that indisputably separates one condition from the others, nor does it underscore the fact that immunologic mechanisms for some of these disorders are incompletely understood. "Senior Clinical Instructor, Department of Pediatrics, Tufts University School of Medicine; Director of Pediatric Allergy, St. Elizabeth's Hospital, Boston, Massachusetts.
Pediatric Clinics of North America-Vol. 16, No.1, February, 1969
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Table 2.
A.
BERMAN
Eczematoid Dermatoses*
Atopic dermatitis Seborrheic dermatitis Contact dermatitis Eczematoid dermatoses of bacterial and fungal origin Nummular eczema Circumscribed neurodermatitis Combinations of the above
* From
Glaser,
J.
G.: Allergy in Childhood. Springfield, Ill., Charles C Thomas
1956.
ATOPIC DERMATITIS
AtopiC dennatitis, a specific clinical entity, occurs at any age, more often in the first few years of life, follows a capricious course, tends to clear with increasing age, and is difficult to manage. The chief problems are based on specific morphologic, physiologic, immunologic, and psychosomatic data and are concerned with control of itching and infection, manipulation of the diet, hyposensitization therapy, and supportive counseling for the parents or the child. There are a number of specific characteristics of the child with atopic dennatitis. Probably the best known peculiarity of these patients is the site of involvement: the flexural areas, face, neck, and extensor surfaces of the arms and legs. Family history of allergy, eventual development of respiratory allergic disease, white dermographism, abnormal disturbances in the delivery of sweat, vascular abnormalities, dry skin, atopic cataract, and dramatic responses to changes in climate and season have all, at one time or another, been described as peculiar stigmata of this disorder. Most authorities agree that atopic dermatitis begins early in life, that many of these patients eventually develop signs and symptoms of respiratory allergic disease-hay fever and asthma-and that the most important aspect of the allergic survey is an accurate and detailed history. At this point, agreement tenninates. The relationship be~een immunologic and clinical information requires further clarification. Some question the need for skin tests in this disorder, citing the lack of correlation between the clinical data and immunological infonnation acquired from direct skin testing. 6 • 7 The patient with this disorder, not unlike the one with hay fever or asthma, may have a great many skin reactions to a variety of antigens, including foods and inhalant substances, many of which are unrelated to his symptoms. It is therefore imperative for allergists to be able to sort out false positive as well as false negative skin reactions, both with foods and inhalants, before attempting to assess their roles in atopic dermatitis. Foods Despite the confusion regarding the relative value of skin tests for uncovering food allergy, it is my opinion that foods can be an important
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contributing cause of atopic dermatitis, particularly in infants and probably less so in the older child and adult. In one study it was observed that such foods as milk and eggs were partly or wholly responsible for atopic dermatitis. Glaser,3 investigating the hypothesis that a milk substitute, such as soy, might limit the development of atopic dermatitis in potentially allergic infants, found that there was indeed a lowered incidence of atopic dermatitis in the soy-fed infants. His study also demonstrated that subsequent respiratory allergic disorders were substantially reduced. The physician should, therefore, seriously consider the dietary management of this disease. Restricted or "elimination" diets are not easy for mothers to initiate or for children to follow. When an elimination diet is to be initiated, the physician should explain as thoroughly as possible the purpose of such a diet, give no assurance that the diet will result in improvement, so construct the diet as to provide satisfactory nutritional intake for the child, and finally assure the parents that the diet is for a limited time. The construction of an elimination diet depends in part on a detailed history, as well as the age of the child. For the patient younger than 6 months of age, elimination diets are usually easy to administer and are worthy of trial. The diet in Table 3 excludes the well-known foods with a high potential of allergenicity, including milk, eggs, wheat, citrus, chocolate, fish, and pork. If, as a consequence of this diet, the eruption is not lessened, then it can be assumed that no sensitization to specifIc foods is present. If the rash is improved, then one new food is added to the Table 3.
Diet Instructions*
For a period of 2 weeks the child's diet is to be strictly limited to the foods listed. He may have any combination of these foods and as much as he wants, but he may not have any other foods unless they are made up of these ingredients. If there is any question about any food, do not use it. Be sure to have everything on hand before starting this diet. Beverages: Soybean milk, containing protein from no other source (such as Neo-Mullsoy, Isomil, or Pro-Sobee) Meats: Lamb or chicken (must be capon or rooster) Cereals: Rice and barley cereals with soybean milk; Ry-Krisp may be used as a cracker or ground up in a meat grinder and served as a breakfast cereal Fruits: Apples, pears, raisins, pineapples Vegetables: Carrots, string beans, lettuce, sweet potatoes Juices: Of permitted fruits and vegetables Miscellaneous: Water, sugar, salt, apple jelly, cranberry juice, maple syrup, maple sugar, honey, and cane sugar Margarines: Those free from milk are Mar-Parv, Mother's, Nuspread, Willow Run, Diet Mazola, Diet Parkay, Diet Chiffon, and Diet Fleischmann's Mocha Mix, which is a substitute for cream (not milk), may be used, but no other cream substitute is allowed; Dzert Mix is a substitute for whipped cream Be sure to read all labels, as the composition of any food may be changed without notice. Be careful to use no foods containing butter, dried milk solids, or casein (the cheese part of milk).
* From Glaser, J. G.: Allergy in Childhood. Springfield, Ill., Charles C Thomas. 1956.
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diet every 4 or 5 days. If a Hare-up of the eruption is observed with a specific food, it is withheld indefinitely, with the provision that it be tried later to observe its effects. This same procedure is continued until the child is returned to a normal diet, excluding, of course, any foods causing exacerbations of the dermatitis. For the older child, or the adult, the same general principles of dietary management are followed, but only if the physician deems such a diet necessary. That elimination diets can be overemphasized and abused is well known. There is nothing more pathetic than to see in consultation an older child with serious atopic dermatitis, burdened by a prolonged, unpalatable restricted diet that is no help whatsoever, and, furthermore, suffering from serious psychological impairment because of the very nature of the diet. In older children and adults, it is much less likely that food sensitization is responsible for the skin lesions of atopic dermatitis. Dietary manipulations should be considered only in the more seriously involved patient, unresponsive to the well-known and accepted modalities of therapy. Inhalants Allergic reactions to inhalants, including sensitivity to pollens, dust, animal danders, and molds, have been implicated as a cause of atopic dermatitis. 4 When an inhalant allergen is suspected of aggravating the disease, the preferred method of tr~atment is, first, avoidance of the offending allergen. This is of particular importance and practical value in those cases in which there is intimate contact with animal danders of all kinds, including wool, cats, dogs, feathers, and parakeets, as well as excessive exposure to dust and molds. If avoidance or reduction of exposure is unattainable, as in the case of dust, molds, or pollens, and there appears to be a reasonable correlation between the clinical phenomenon and the skin tests, then hyposensitization therapy is indicated, particularly if the atopic dermatitis is of moderate or serious intensity. When resorting to hyposensitization therapy, meticulous cai-e is required, so that the dose of the specific extract will not exceed the limit of tolerance of the patient, for when this occurs, the atopic dermatitis is apt to be made worse. There is, however, another reasonable and practical aspect of reducing or avoiding contact with inhalant allergens, and that is that continuous exposure to and contact with potent inhalant allergens may lead to future sensitization and be partly or wholly responsible for the development of respiratory allergic syndromes, which are likely to occur in at least 40 per cent of all children affiicted with atopic dermatitis. Contactants Certain types of irritative garments, such as wool, can act as nonspecific irritants and perpetuate the inHammatory process of atopic
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COMMON DERMATOLOGIC CONDITIONS
dermatitis. However, whether wool as such, acting against the skin, can, by specific sensitization, initiate the lesions of atopic dermatitis remains unanswered. Topical Therapy
Changes in the skin vary in the acute phase from mild erythema with scaling to oozing, with or without infection. In the chronic state, lichenification, with or without depigmentation, is prominent. Itching, which is the most profound and disturbing of all the symptoms, is generally more prominent after bedtime. Lack of sleep as well as general discomfort produces irritability, fretfulness, and loss of appetite. The usual signs and symptoms of infection may not be apparent when the patient is examined. Careful inspection for a solitary pustule, enlarged regional lymph nodes, or a history that the mother, or another child, is afflicted with a skin infection, may tell a good deal about infection in the patient. In mild cases, in which there is minimal erythema and scaling, simple measures usually suffice for suppressing the disorder. The most effective agents are the corticosteroid creams. For that matter, the single most important advance in the treatment of eczema during the past 20 years has been the advent and development of the corticosteroid hormones. Cort-Dome, Valis one, Synalar, or Kenalog, whose effects are enhanced considerably if the medicament is applied at least 10 times a day, is applied thinly and rubbed in vigorously to the affected areas. When there is improvement, the number of applications of corticosteroid cream is rapidly reduced. A modification of Rosen's ointment, which may be considered by some to be outmoded in the current steroid era, may be surprisingly helpful in many instances. This preparation is as follows: Burow's solution Polysorb Lassar's paste q.s. ad Sig.: Apply 4 to6 times a
10 20 60 day
For those patients whose lesions are oozing or weeping, nonirritating soaks with Burow's solution, prepared by dissolving one Domeboro tablet or powder in a pint of cool water, are carefully applied. Although any soft fabric may be used for applying a soak, an effective method is the use of cheesecloth. After a pack containing 20 layers or more of cheesecloth has been soaked in Burow's solution and placed over the affected area, a bath towel is wrapped around the moist dressings. A large sheet of plastic is placed under the child to protect the bedding and can, if desired, be used to hold the dressing in place. The pack should be kept moist and in place for as long as the child can tolerate it, which in most cases is not more than 20 minutes at one time. During the interval when
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the packs are removed, or during sleeping hours, Rosen's modified ointment or one of the various corticosteroid creams can be applied. Colloidal baths are soothing and anti-inflammatory and can be substituted twice or more a day for wet dressings. Laundry Linit, a commercial starch preparation, 2 cupfuls to a tub of water, is inexpensive and satisfactory, while Aveeno bath serves the same purpose. For lichenified lesions, tars with or without corticosteroid hormones are effective. For thickened lesions with associated infection, the quinolones are particularly useful. For chronic thickened lesions: Prescription 1: Liquor carbonis detergeris 1.80 Salicylic acid 3.00 Neobase q.s. ad 60.00 Sig.: Apply to affected areas 4 to 8 times a day Prescription 2: Cor-Tar-Quin 0.5% Sig.: Apply to affected areas 6 to 10 times a day Prescription 3: Vioform powder 1.80 Liquor carbonis detergens 1.80 Synalar (0.10%) 15.00 Lassar's paste i q.s. ad 60.00 Sig.: Apply to affected areas 6 to 10 times a day
Occlusive dressings may be utilized. Although the results are unpredictable and in some cases the eruption may even Hare, there is enough merit in this technique to deserve consideration as an important modality of therapy, particularly if the lesions are below the elbows and knees and are in the subacute or chronic stage. Any of the corticosteroid creams, such as Synalar, Cort-Dome, Kenalog, or Valisone, is applied sparingly to the lesions, rubbed in vigorously until the cream disappears, and then covered with a thin, pliable, noninflammable, transparent, moisture-retaining material, such as Saran Wrap or even a Baggie (small .. plastic bag.) When a plastic material is used, it is imperative that the bag be of such a small size as never to fit over a child's head, because of the danger of suffocation. For the hands, a plastic glove is ideal. When the open ends are sealed with 3 M Blenderm tape, an airtight compartment is provided, which prevents evaporation of moisture and in tum can promote rapid healing of the lesions. Occlusive dressings are applied at bedtime and removed in the morning. Localized infections are treated much the same way as an oozing wet lesion. Soaks with Burow's solution are used along with topical antibiotics, such as Bacitracin, Bacirnycin, Neopolycin, Neosporin, or Vioform. Dermatologic preparations that contain sulfa or penicillin are to be avoided, because sensitization reactions frequently result from their use. When there is evidence of spreading infection, or signs or symptoms of pustular or irnpetigenized areas, antibiotics, chosen by the results of
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culture and sensitivity, are administered systemically along with wet dressings. Antihistamines Antipruritic therapy is essential for the management of atopic dermatitis. Although the antihistaminics are said to be potent antipruritic agents, control of pruritus using these medicaments is often less than satisfactory. It is also impossible to anticipate a patient's reactions to these drugs, because antihistaminics vary considerably in side effects and clinical response. Therefore the choice of an antihistaminic agent is usually made after experimenting with a number of preparations. The following antihistaminic agents may be used as directed, but the dosage may have to be lowered or increased according to the requirements and tolerance of the patient, or, because of ineffectiveness, another antihistaminie may have to be tried. Elixir of Benadryl or Phenergan Fortis are usually excellent choices for dispensing at bedtime, because they generally produce not only an antipruritic response, but also a strong sedative and, at times, a soporific effect. For a child aged 1 year, 3 teaspoons of Elixir of Benadryl, or Y2 teaspoon of Syrup of Phenergan Fortis, is offered. For the older child, Elixir of Benadryl may be increased to 4 teapsoons and Phenergan Fortis to 1 teaspoon. Anyone of the following can be prescribed as a daytime antihistaminic, in a dose of Y2 to 1 tablet, or teaspoon, three times a day: Chlor-Trimeton, Periactin, Actifed, Tacaryl, Dimetane, or Pyribenzamine. Aspirin, in the usual doses for children, is at times an effective antipruritic agent which can be taken alone or along with an antihistaminic. Other Medications Tranquilizing agents are occasionally beneficial in the treatment of atopic dermatitis, because they relax the patient and thus reduce pruritus and scratching. Some tranquilizing agents are even more helpful because of additional antihistaminic effect. An example of this is Syrup of Atarax, which is offered in a dose of 1 to 2 teaspoons three times a day. As a substitute for an antihistaminic, and particularly when sedation is desirable, chloral hydrate may be dispensed as Noctec, 1 to 2 teaspoons, at bedtime. Noctec contains 7.5 grains of chloral hydrate per teaspoon. Unfortunately, the response to phenobarbital has been extremely disappointing, because its actions are unpredictable; more often than not, the child is stimulated. It is suggested that soaps of all kinds be avoided during the acute phase of atopic dermatitis. However, pHisoHex is particularly useful in the acute stage and also if the skin is infected. Nonallergenic soaps, such as Aveeno-Bar, Lowila Cake, or Neutragena, all of which are nonkeratolytic and have a pH that approximates that of the skin, are suggested for subacute or chronic stages of atopic dermatitis.
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For softening dry skin, which may be responsible for pruritus and scratching, applications of specific medicaments are recommended. Examples of skin softeners are Alpha Keri, Domol, and Ar-Ex Bath Oil, all of which require 2 capfuls to a tub of water. Also of value are various skin softeners, which are applied after a bath. Effective and cosmetically acceptable are Keri Lotion, Ar-Ex Body Lotion, and Allercreme Special Formulated Skin Lotion. Unfortunately, with the availability of topical corticosteroid hormones, which have simplified the treatment of this disorder, there has been a tendency to neglect other equally important areas of therapy. For example, when there is extensive skin involvement, particularly involving the extremities, a practical measure is to apply a loose white cotton covering, or a bandage, enclosing the affected area. This serves to protect the skin from irritants, such as garments or rugs, which through frictional contact increase itching and aggravate lesions. Furthermore, maceration of the skin by an infant who crawls on rugs or floors can be minimized by such a simple protective covering. Corticosteroid Honnones Systemic corticosteroid hormone therapy may be needed as shortterm treatment for severe disseminated atopic dermatitis. Although no one particular cortisone derivative is more effective than any other, prednisone, because it is less expensive, is usually prescribed, in a dose of 30 to 50 mg. for the first 24 to 48 hours. At th6l end of this time, if there is improvement, the prednisone is gradually reduced, so that no more is given by the seventh day. The corticosteroid hormones are prescribed along with all the other modalities of topical therapy. If the patient is no better, then hospitalization may be necessary. Needless use of systemic corticosteroid hormones is contraindicated, particularly when other avenues of treatment will suffice for control of the disorder. Furthermore, long-term daily use of suppressive doses of corticosteroid hormones is ill-advised, because of the well~Imown sequelae and complications. However, there are instances of hard-core intractable eczema, and long-term steroid therapy can, by judicious use, convert a totally disabled child, both physically and emotionally, to one who is able to be comfortable, to sleep well, feel well, and participate in normal school and play activities. If there is a need for continuous steroids, then the alternate day administration of corticosteroid hormones, if effective, is the treatment of choice. Side effects from alternate day steroids are minimal; the child usually grows normally, and adrenal function is not appreciably altered. Because of their characteristic rate of excretion, dexamethasone, triamcinolone, and betamethasone are not suitable for alternate day administration. Used in this manner, these agents quickly produce signs and symptoms of steroid overdosage. I have observed that prednisone is the most satisfactory corticosteroid for alternate day therapy. The drug is administered initially in higher
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dosage, reduced quickly as the rash improves, and continued as a single dose, after breakfast, every other day. In some instances, children have been made comfortable with as little as 5 to 10 mg. of prednisone, while a few patients have required as much as 20 to 25 mg. for adequate control. With careful patient selection, with an appreciation of side effects, and exercising sound judgment for prompt withdrawal when no longer needed, corticosteroid hormones, whether used for short-course daily treatment or for longer-term alternate day administration, are important additions in the care of atopic dermatitis. Instructions for the care of a small child with atopic dermatitis are as reproduced as Table 4. Table 4.
Sample Instruction Sheetjor Home Care oj an 18-Month-Old Child with Atopic Dermatitis
Please follow these instructions carefully; the directions given under Plan A are to be followed daily. The vaporizer need not run all day-only when the child is put to bed at night. Be sure to add sufficient water that the vaporizer will be effective during the time that the child is sleeping. If the eruption flares, in addition to continuing with all the items in Plan A, go to Plan B. Apply cream No.1 thinly and evenly and rub it in vigorously. If the eruption is intensified or appears more irritated after application of the cream, stop applying it promptly and call this office immediately. As soon as the rash has improved dramatically, diminish the frequency of application to once or twice a day. If there are signs or symptoms of infection, a matter we have previously discussed with you, use cream No.2 in place of cream No. 1. The directions for the use of cream No.2 are the same as for cream No. 1. If eczema involves the hands or feet, try Plan C. If the symptoms appear to be worse, discontinue Plan C promptly. If, after following these instructions, the patient's skin is no better, please call the office for further instructions. Plan A: Care of the Skin Neutragena (substitute for soap) Alpha Keri, 2 capfuls to a tub of water Cold mist vaporizer Elixir of Benadryl, 1 tablespoonful at bedtime ChI or-Trimeton, ~ teaspoonful morning and noon Allercreme Special Formulated Skin Lotion, after bath as a skin softener Plan B: If the Eruption Flares Cream No.1: Cort-Dome Cream, ~% .. Apply 10 times daily thinly to affected area and rub in vigorously. Cream No.2: Neo-Cort-Dome Cream, ~%. Apply 10 times daily thinly to affected area. Plan C: For Rash of Hands or Feet Cort-Dome Cream is spread thinly and rubbed in vigorously over the affected area. Saran Wrap .covers the lesions to form an airtight compartment. The ends are sealed with Blenderm, a nonallergenic tape. The Saran Wrap is applied at bedtime and removed in the morning.
Humidification Serious harm to the mucous membranes of the respiratory tract, as well as the skin, can result from excessively dry air. This problem is especially troublesome and common in temperate climates, usually in the winter months and in those homes where central heating is required
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continuously for many months each year. Most homes in cold weather have relative humidities ranging from 10 to 15 per cent, probably with lesser percentages recorded where the heating is through duct systems. Ideally, a relative humidity of 30 to 40 per cent is recommended, but this is often unattainable even with central humidifiers in those sections of the country where temperatures outside the home rarely rise above 10° F. Dry heated air acts as a sponge, soaking up moisture and drying the skin and mucous membranes of the respiratory tract, and is particularly injurious to those patients afHicted with atopic dermatitis or respiratory allergic disorders. Excessive dryness of the skin frequently is responsible for pruritus, even without the presence of atopic lesions. Therefore adequate humidity in the home is a prerequisite for the proper care of the child with atopic dermatitis, for, by its effect of keeping the skin moist and soft, pruritus may be markedly lessened. An important byproduct of sufficient moisture in the air is that it reduces brittleness of various fabrics in the home, thus lessening dust and lint formation. Cool mist humidifiers range in size from small, inexpensive room appliances to more sophisticated and expensive central humidifiers, for which one must have a duct system. For the single room the Hankscraft or similar DeVilbiss apparatus is practical. For humidification of larger areas of the home and where there is no duct system available, a larger console humidifier is practical. Examples of this type are Arvin, Walton, and Sunbeam. Immunization Most physicians are aware of the untoward and serious effects .of herpes simplex and vaccinia virus. In patients with atopic dermatitis, both can produce the syndrome of Kaposi's varicelliform eruption. Apparently, atopic dermatitis lowers the host's resistance to these viruses. For those whose eruption is caused by the vaccinia virus, there is available a specific vaccinia-immune gamma globulin preparation, which, when administered in proper dosage! (1 ml. per kg. of body 'weight) can be extremely effective and, at times, life-saving. In the presence. of atopic dermatitis, vaccination of the patient or other members of the family is contraindicated, and close contact with other vaccinated children is forbidden. SEBORRHEIC DERMATITIS
Seborrheic dermatitis, the most commonly encountered dermatitis of infancy, is a disorder of unknown origin, most often a benign, self-limited eruption, but at times chronic and often confused with and misdiagnosed as atopic dermatitis. Seborrheic dermatitis is characterized by two principal forms. One is a scaly eruption (scales may be dry or greasy) on an inflammatory base, affecting chiefly the scalp, eyebrows, eyelids, upper
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COMMON DERMATOLOGIC CONDITIONS
portion of the face, pubic regions, and presternal areas of the trunk. Another form, intertriginous, is usually moist and involves the postauricular, axillary, and inguinal areas, as well as other flexural areas. Table 5.
Differential Diagnosis Between Atopic Dermatitis and Seborrheic Dermatitis* ATOPIC DERMATITIS
Family history of allergy Skin tests Pruritus Eosinophilia Association with respiratory allergies General distribution
Usually positive
Not so commonly positive
Positive reaction to foods and inhalant allergens Always present
Usually negative
Nasal and blood eosinophilia are common %: of all patients The face, flexor surfaces of the upper and lower extremities, dorsal surfaces of the arms and legs
Color, shape, and nature of eruption
Scales are white, usually not large, and the edges rarely curl; serpiginous outlines are rare; erythema, scaling, oozing, crusting, and secondary infection, as well as lichenification, are common
Scratch marks Secondary infection Depigmentation Flexor involvement
Very common Common Common Lichenification prominent in chronic lesions; creases of flexural surfaces of arms are involved, and the process frequently extends up and down the forearm quite a distance; the same distribution is frequently noted on the lower extremities Lesions mayor may not be present
Scalp
Injection therapy Elimination diet Prognosis
* From 1956.
SEBORRHEIC DERMATITIS
Glaser,
Sometimes helpful Sometimes useful Guarded
J.
May be present, but is rarely as severe as atopic dermatitis Rarely present Less than
~
of all patients
Chiefly the scalp, eyebrows, eyelids, along the hairline, and upper portion ofthe face; occasionally cheeks, pubic region, and presternal area of the chest; intertriginous involvement of the posterior auricular, axillary, and inguinal areas Body lesions are often in the shape of waxy plaques that appear yellow when the skin is tensed; frequent greasy scales, "potato chip" in appearance, with edges that curl; coalescent large lesions with serpiginous borders; moist lesions in intertriginous areas Rare Rare Does not occur No lichenification; flexor lesions are confined to the skin surfaces that touch one another; for that matter, the eruption typically occurs wherever the skin surfaces come together, e.g., in fat folds of the abdomen and elsewhere Typical cradle cap always due to seborrheic dermatitis, never atopic dermatitis Not needed Never useful Practically always good
G.: Allergy in Childhood. Springfield, Ill., Charles C Thomas,
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It has been suggested that seborrheic dennatitis is a forerunner of atopic disease, because a small percentage of patients with seborrheic dennatitis will gradually develop the skin eruption consistent with a diagnosis of atopic dennatitis. Also, the two disorders frequently coexist. Prompt treatment of seborrheic dennatitis will not prevent the development of atopic dennatitis. Because there are many infants with seborrheic dennatitis who never develop atopic dennatitis, it is important to make an accurate differential diagnosis between these two disorders (Table 5). As a rule, the patient with seborrheic dermatitis has little or no pruritic involvement, has negative skin tests, and rarely develops subsequent respiratory allergic diseases. Therefore there is no reason for skin tests, elimination diets, or hyposensitization therapy, nor a need to induce anxiety in parents who dread the diagnosis of atopic dennatitis.
Treatment For seborrheic involvement of the scalp, a variety of shampoos are available and are usually effective. All these preparations are potential irritants and should be discontinued promptly if undue skin irritation is present. The hair is shampooed at least twice a week. Any of the following may be used as a shampoo and the directions are the same for all: Fostex Cream, Sebutone, or Sebulex. Massage a liberal amount of the preparation into the wet scalp for 3 to 5 minutes, rinse, repeat, then rinse thoroughly once again. After shampooing, apply one of the following at least twice a day: Neo-Synalar, Cordran-N, Synalar Solution, Kenalog-N, or Neo-Cort-Dome. For stubborn cases involving the scalp, one can turn to some of the older and established therapeutic preparations, which may help. The following is an! example: Salicylic acid 1.80 Sulfur ppt ..• 2.00 Neo Base q.s. ad 60.00 Sig.: Rub into the scalp 2 or 3 times a week at night and wash out the next day
Pragmatar or Packer Tar Shampoo is also useful. If these medicaments prove ineffective for removing thickened scalp lesions, then an occlusive technique may be surprisingly helpful. After applying a tar shampoo and rinsing thoroughly, one of the aforementioned corticosteroid creams is rubbed in liberally and vigorously, covered by Saran Wrap, and kept in place by a shower cap tied loosely under the chin. The occlusive dressing is applied at bedtime and removed in the morning. This procedure, which may have to be repeated several times before there is improvement, is not suitable for infants or young children because of the potential hazards of plastic material near the face.
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For lesions of the body, Vioform ointment, Vioform hydrocortisone, Cordran-N, Kenalog-N, Neo-Cort-Dome, and Neo-Synalar are all excellent preparations. For marginal blepharitis, believed to be of seborrheic origin, 10 per cent sodium sulamyd ointment is useful. Erythroderma desquamativum (Leiner's disease) is a generalized and intensified form of seborrheic dermatitis. Treatment is the same as for the milder forms of seborrheic dermatitis. If topical steroids need to be used, but are of no help, then a short course of oral corticosteroids may have to be utilized. Petrolatum, with or without salicylic acid, 5 grains to the ounce, is often of some help. pHisoHex is useful to reduce secondary infection. These babies can run a stormy course, so that hospitalization is frequently necessary. Severe gastrointestinal disturbances, particularly diarrhea, are cardinal features of this disorder. Correction of dehydration, maintenance of adequate nutritional intake, and control of diarrhea and infection are best accomplished in a hospital setting. In this country, unlike Europe, this disease is rare. Its duration is usually not over 3 months, recovery is permanent, and there are no sequelae.
CONTACT DERMATITIS
Contact dermatitis, a common and troublesome disorder, is mediated by a delayed hypersensitivity reaction. The diagnosis is suspected by history, morphology, and distribution. A multitude of different sensitizing agents can be responsible for the eruption, including chemicals, jewelry, drugs, cosmetics, and plastics. The list is limitless and, of course, must include members of the plant kingdom. By far the most common contact allergic eruption from plants is caused by poison ivy, poison oak, or poison sumac, all included under the generic botanical term Rhus. It is important for the physician to realize that not all plant dermatitis is caused by poison ivy or its biologically related plants. Although less frequently involved as causative factors, the following can induce contact dermatitis: primrose, chrysanthemum, ragweed, a variety of trees and grasses, as well as large numbers of fruits and vegetables. When sensitization is established, the changes in the skin may range from mild erythema with scaling to vesiculation, oozing, bullae, and even lichenification. Pruritus is usually intense. Patch tests are typically positive, while scratch and intradermal tests are almost always negative. The symptomatic treatment of contact dermatitis is essentially the same as for atopic dermatitis. Poison Ivy (Rhus toxicodendron) A few additional comments regarding poison ivy are essential. The sensitizing factor, an oleoresin, is contained in the sap of the leaves.
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Contact is made either by touching the plant, by standing nearby when the leaves are being burned, or by patting a dog or cat that carries the active sensitizing fraction-or even by handling contaminated garments, logs, or other plants. Characteristically, several days after contact with the sensitizing fraction, the patient develops vesiculation, erythema, marked edema, oozing, and moderate to severe pruritus. Vesicles are often distributed in linear fashion. The exposed areas of the body are quick to develop eruptions, followed in a few days, in some instances, by involvement of other remote skin areas. It is important to remember that the serous exudate from the lesions does not contain the active sensitizing fraction, and represents only the inHammatory response of the host to poison ivy. Because the oleoresin of poison ivy is gluelike, it can remain fixed to the skin, still capable of sensitizing, for several days or longer. Therefore it is advisable that unaffected areas of the skin be scrubbed vigorously and involved sites washed gently with soap and water. All clothes suspected of being contaminated should also be cleansed thoroughly. For local and minimal involvement of the skin, soaks, orally administered antihistaminic agents, and topical corticosteroid creams are sufficient. For the patient with intense local or generalized poison ivy dermatitis, or for that matter severe contact dermatitis from other causes, orally administered corticosteroids are the treatment of choice. Calamine lotion and liniment are of little or no help. Tap water soaks and optimum doses of antihistaminics, administered along with corticosteroid hormones, will lessen the intensity of the eruption in about 48 hours. Prednisone, 2 mg. per kg. per 24 hours, is the preferred corticosteroid preparation. However, satisfactory results will usually follow if prednisone is administered in a dose of 50 mg. on the first few days and then, as improvements follows, is rapidly reduced, so that no more is given by the seventh or eighth day. Attempts have been made to prevent poison ivy sensitivity (as well as that of poison oak and poison sumac) by injection of alum-precipated pyridine extracts of poison ivy (Dome Chemical Co.) given well in advance of the season. Others have resorted to oral preparations of a poison ivy extract (Hollister-Stier Laboratories, Inc.) to provide protection. Beneficial results from the use of these products have been reported. Others refer to their placebo effect, describing them as worthless. Ii In any event, if hyposensitization is contemplated, it should be utilized only for the most sensitive patients, specifically those who have serious eruptions year after year, despite all attempts to avoid contact with the plants. These preparations are not without side effects. They should be discontinued promptly, then restarted at lower dosage, if dermatitis or pruritus ani (not uncommon with oral extracts of poison ivy) are observed, and they should never be administered in the presence of clinically apparent poison ivy.
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207
URTICARIA
Urticaria, a common a:ffiiction, is characterized by localized or generalized crops of wheals, usually evanescent, associated with itching and burning and sometimes involving mucous membranes of the respiratory and gastrointestinal tracts. Urticaria (or hives) results from the influence of one or more chemical mediators upon the capillaries or venules. If the individual urticarial lesion is extensive and marked by intense edema, it is termed angioedema. Not all urticaria is allergic. When allergenic factors are involved, the condition usually results from a reaction of the specific allergen with its corresponding antibody, which releases one or more chemical mediators, which in tum act on the capillary bed. Nonallergenic causes are equally important in the development of hives, which may be present as an acute self-limited disorder, or a chronic relapsing condition. The patient is said to have chronic urticaria when the process has been present for weeks (usually 4) to months. Chronic urticaria, occurring far less often in children than in adults, is often difficult to manage. Determining the cause of hives is frequently a tedious and complex procedure. Table 6 is an oversimplified chart demonstrating the multitudinous origins of this disorder. In children, hives generally occur as an acute, self-limited process, and often cannot be related to anyone causative factor. When a cause can be isolated, the most likely ones are acute infection, drug allergy, ingestion of a specific food, or inhalant allergy to pollens, animal danders, or miscellaneous allergens. In children, chronic hives involving the extreInities should raise a suspicion of papular urticaria; when hives are linear, dermographism is the most likely explanation. Sensitivity to foods should be given serious consideration when caring for a patient with chronic urticaria. In most instances, scatch or intradermal tests for foods are of little or no help in identifying the responsible allergens. If skin tests are negative, elimination diets, coupled with food diaries, are the choice of management. For a complete discussion of the technique of administration of elimination diets, the reader is referred to the section on "Atopic Dermatitis." The· offending foods are many, but it is generally agreed that milk, eggs, pork, chocolate, nuts, fish, shellfish, and fruits are the most common offenders. Reproducible evidence of hives occurs within seconds to several days after the ingestion of the offending food. Drug-induced urticaria is complicated by the fact that the patient or parent often does not volunteer or admit to taking drugs unless specifically questioned. There is no intentional withholding of information, but many do not appreciate or consider that cathartics, tranquilizers, weight-reducing agents, and aspirin fall into the category of drugs.
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Table 6.
A.
BERMAN
Etiology oj Hives
1. Ingestion of specific foods, coloring agents or fillers in foods, such as nuts, chocolate, fish, lobster. 2. Inhalant allergens: animal danders, including dogs and cats, or pollen urticaria, often called seasonal hives, caused by exposure and sensitivity to the various pollens of trees, grasses, and weeds. 3. Drug allergy, including all drugs. Most common, however, is penicillin (even the traces of penicillin found in cow's milk as a result of treating infected udders with this drug). 4. Papular urticaria-common on the extremities and thought to be due to sensitivity to bites of bedbugs, fleas, mites, or mosquitoes. Lesions are both papular and urticarial, are intensely pruritic, and often are infected because of scratching. 5. Hymenoptera sting-systemic reaction resulting from the bite of a bee, wasp, yellow jacket, or hornet (there is a similar reaction from an ant bite, but this occurs rarely). Prevention of recurrence of systemic reaction is essential and is accomplished, in most instances, by injection therapy with extracts containing equal parts of b("e, wasp, yellow jacket, and hornet. Hyposensitization continues for 3 years or longer. 6. As a consequence of injection therapy for the treatment of inhalant allergies-overdose of pollen produces systemic reaction, associated in part with urticaria. 7. Injection of antisera (horse serum), such as tetanus antitoxin; when fever and swelling of the joints are also present, the process is called serum sickness. 8. Infection, acute or chronic (viral or bacterial). 9. Parasitic infestation. 10. Cholinergic urticaria, following exposure to heat, exercise, or emotion and sometimes reproducible by injection of cholinergic drugs. Lesions are pea-sized and discrete. 11. Urticaria occurring after contact with water of any temperature; even noted with patient's own sweat. 12. Physical factors, including cold, heat, and light. There is some evidence that physical allergy may be mediated on an immune basis, because in some cases the process may be passively transferred. 13. Hereditary angioneurotic edema. Laryngeal edema is common and accounts for the high mortality in this disorder. These patients lack serum inhibitors of an enzyme derived from the first part of complement. 14. Agents or drugs that release bound histamine, including morphine, codeine, certain toxins, and venoms (snake bites). 15. Dermographism. Reaction caused by gentle stroking of the skin. Usually produces whealing in linear form. Frequently confused with hives of immune origin. 16. Urticaria pigmentosa. Patients have, scattered over the trunk, isolated or multiple brown or yellowish brown macules about 1 cm. or larger in diameter. Rubbing the lesions produces localized urticaria (Darier's sign). The lesions on the skin are conglomerates of mast cells which release histamine when traumatized. Similar clusters of mast cells may occur in other organs. 17. Urticaria associated with morbid systemic diseases: lymphoma, leukemia, and systemic lupus erythematosus. 18. Urticaria caused by endocrine disorders-pregnancy; menses; thyroid disease. 19. Emotionally induced urticaria.
Therefore, in history taking, it is important to elicit each of the medicaments ingested by the patient. It is not sufficient to ask the patient, "Are you taking any drugs?" Physical causes of hives are the subject of renewed interest. Cold urticaria is of particular concern because of possible accidental death occurring under certain circumstances. Swimming in cold ocean water induces urticaria, and if the precess becomes intense and generalized, syncope and drowning may occur.
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The most effective management of urticaria, whether acute or chronic, depends in a large measure on finding the cause-which, however, is not always possible. Symptomatic treatment relies chiefly on the various antihistaminic preparations. In my experience, Atarax has been the most consistently effective preparation. The dose of Atarax should be pushed to tolerance, or control of symptoms, whichever occurs first. In a few instances, as much as 50 to 100 mg. three times a day is required to suppress the eruption. For disseminated urticaria, either acute or chronic, and unrelieved by optimum doses of antihistaminic preparations, injectible agents, such as epinephrine or Benadryl (1 mg. per kg., not to exceed 40 mg. per single dose) administered subcutaneously, may help. Short courses of corticosteroid hormones may be needed for severe cases. When there is laryngeal edema, prompt and vigorous treatment with subcutaneous epinephrine, or even tracheostomy, is necessary. Injection therapy with appropriate allergens may help if pollens or miscellaneous allergens, such as dust or molds, are the responsible agents. When hives result from drug or food ingestion, or exposure to animal danders, and the specific causative factor can be uncovered and removed, improvement is likely to occur.
ACKNOWLEDGMENT
The author wishes to thank Dr. Jerome Glaser of Rochester, New York, for permission to use material from his book.
REFERENCES 1. Gellis, S., and Kagan, B., eds.: Current Pediatric Therapy III. Philadelphia, W. B. Saunders Co., 1968. 2. Glaser, J. G.: Allergy in Childhood. Springfield, Ill., Charles C Thomas, 1956. 3. Glaser, J. G.: The prophylaxis of allergic disease in infancy and childhood. Acta Paediat., 46:43, 1957. 4. Hill, L. W.: The Treatment of Eczema in Infants and Children. St. Louis, C. V. Mosby Co., 1956. 5. Kanof, N. B., and Baer, R. L.: Attempts to hyposensitize with poison ivy extracts. Ann. Allergy, 22: 161, 1964. 6. Rostenberg, A., Jr.: Atopic dermatitis: A discussion of certain theories concerning its pathogenesis. In Baer, R. L., ed.: Atopic Dermatitis. New York, New York University Press, 1955, p. 65. 7. Stifler, W. C., Jr.: Conference on infantile eczema. J. Pediat., 66:235, 1965.
1714 Beacon Street Brookline, Massachusetts 02146
The allergic dermatoses, comprising a lengthy list of skin disorders commonly encountered in the day-to-day practice of medicine, present a distinct and singular challenge to the physician involved with their diagnosis and subsequent management (Table 1). Of all these derTable 1.
Allergic Dermatoses (Cutaneous Allergic Reactions)
Eczematoid dermatoses Urticaria Drug eruptions Physical allergy Allergic purpura Reactions associated with acute or chronic infection Reactions associated with autoimmune or collagen disorders
matoses, the most prevalent ones, which bother the physician the most, are the eczematoid dermatoses, commonly referred to simply as "eczema." It can be said of eczema that it is a stubborn skin eruption, characterized by erythema, scaling, oozing, lichenification, or any combination of these, and occurring in subacute, acute, or chronic forms. The eczematoid dermatoses, in effect, constitute a group of skin disorders with some, but not all, features in common. It is not possible in this article to discuss all these disorders fully and completely, and the reader is referred to standard texts. We will highlight a few of the more common and troublesome ones. Our classification (Table 2) is accurate enough in descriptive terms for the classic types, but it ignores the many etiologic components that are present in each case. It does not consider the fact that there is no completely defined pathologic difference that indisputably separates one condition from the others, nor does it underscore the fact that immunologic mechanisms for some of these disorders are incompletely understood. "Senior Clinical Instructor, Department of Pediatrics, Tufts University School of Medicine; Director of Pediatric Allergy, St. Elizabeth's Hospital, Boston, Massachusetts.
Pediatric Clinics of North America-Vol. 16, No.1, February, 1969
193
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Table 2.
A.
BERMAN
Eczematoid Dermatoses*
Atopic dermatitis Seborrheic dermatitis Contact dermatitis Eczematoid dermatoses of bacterial and fungal origin Nummular eczema Circumscribed neurodermatitis Combinations of the above
* From
Glaser,
J.
G.: Allergy in Childhood. Springfield, Ill., Charles C Thomas
1956.
ATOPIC DERMATITIS
AtopiC dennatitis, a specific clinical entity, occurs at any age, more often in the first few years of life, follows a capricious course, tends to clear with increasing age, and is difficult to manage. The chief problems are based on specific morphologic, physiologic, immunologic, and psychosomatic data and are concerned with control of itching and infection, manipulation of the diet, hyposensitization therapy, and supportive counseling for the parents or the child. There are a number of specific characteristics of the child with atopic dennatitis. Probably the best known peculiarity of these patients is the site of involvement: the flexural areas, face, neck, and extensor surfaces of the arms and legs. Family history of allergy, eventual development of respiratory allergic disease, white dermographism, abnormal disturbances in the delivery of sweat, vascular abnormalities, dry skin, atopic cataract, and dramatic responses to changes in climate and season have all, at one time or another, been described as peculiar stigmata of this disorder. Most authorities agree that atopic dermatitis begins early in life, that many of these patients eventually develop signs and symptoms of respiratory allergic disease-hay fever and asthma-and that the most important aspect of the allergic survey is an accurate and detailed history. At this point, agreement tenninates. The relationship be~een immunologic and clinical information requires further clarification. Some question the need for skin tests in this disorder, citing the lack of correlation between the clinical data and immunological infonnation acquired from direct skin testing. 6 • 7 The patient with this disorder, not unlike the one with hay fever or asthma, may have a great many skin reactions to a variety of antigens, including foods and inhalant substances, many of which are unrelated to his symptoms. It is therefore imperative for allergists to be able to sort out false positive as well as false negative skin reactions, both with foods and inhalants, before attempting to assess their roles in atopic dermatitis. Foods Despite the confusion regarding the relative value of skin tests for uncovering food allergy, it is my opinion that foods can be an important
COMMON DERMATOLOGIC CONDITIONS
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contributing cause of atopic dermatitis, particularly in infants and probably less so in the older child and adult. In one study it was observed that such foods as milk and eggs were partly or wholly responsible for atopic dermatitis. Glaser,3 investigating the hypothesis that a milk substitute, such as soy, might limit the development of atopic dermatitis in potentially allergic infants, found that there was indeed a lowered incidence of atopic dermatitis in the soy-fed infants. His study also demonstrated that subsequent respiratory allergic disorders were substantially reduced. The physician should, therefore, seriously consider the dietary management of this disease. Restricted or "elimination" diets are not easy for mothers to initiate or for children to follow. When an elimination diet is to be initiated, the physician should explain as thoroughly as possible the purpose of such a diet, give no assurance that the diet will result in improvement, so construct the diet as to provide satisfactory nutritional intake for the child, and finally assure the parents that the diet is for a limited time. The construction of an elimination diet depends in part on a detailed history, as well as the age of the child. For the patient younger than 6 months of age, elimination diets are usually easy to administer and are worthy of trial. The diet in Table 3 excludes the well-known foods with a high potential of allergenicity, including milk, eggs, wheat, citrus, chocolate, fish, and pork. If, as a consequence of this diet, the eruption is not lessened, then it can be assumed that no sensitization to specifIc foods is present. If the rash is improved, then one new food is added to the Table 3.
Diet Instructions*
For a period of 2 weeks the child's diet is to be strictly limited to the foods listed. He may have any combination of these foods and as much as he wants, but he may not have any other foods unless they are made up of these ingredients. If there is any question about any food, do not use it. Be sure to have everything on hand before starting this diet. Beverages: Soybean milk, containing protein from no other source (such as Neo-Mullsoy, Isomil, or Pro-Sobee) Meats: Lamb or chicken (must be capon or rooster) Cereals: Rice and barley cereals with soybean milk; Ry-Krisp may be used as a cracker or ground up in a meat grinder and served as a breakfast cereal Fruits: Apples, pears, raisins, pineapples Vegetables: Carrots, string beans, lettuce, sweet potatoes Juices: Of permitted fruits and vegetables Miscellaneous: Water, sugar, salt, apple jelly, cranberry juice, maple syrup, maple sugar, honey, and cane sugar Margarines: Those free from milk are Mar-Parv, Mother's, Nuspread, Willow Run, Diet Mazola, Diet Parkay, Diet Chiffon, and Diet Fleischmann's Mocha Mix, which is a substitute for cream (not milk), may be used, but no other cream substitute is allowed; Dzert Mix is a substitute for whipped cream Be sure to read all labels, as the composition of any food may be changed without notice. Be careful to use no foods containing butter, dried milk solids, or casein (the cheese part of milk).
* From Glaser, J. G.: Allergy in Childhood. Springfield, Ill., Charles C Thomas. 1956.
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diet every 4 or 5 days. If a Hare-up of the eruption is observed with a specific food, it is withheld indefinitely, with the provision that it be tried later to observe its effects. This same procedure is continued until the child is returned to a normal diet, excluding, of course, any foods causing exacerbations of the dermatitis. For the older child, or the adult, the same general principles of dietary management are followed, but only if the physician deems such a diet necessary. That elimination diets can be overemphasized and abused is well known. There is nothing more pathetic than to see in consultation an older child with serious atopic dermatitis, burdened by a prolonged, unpalatable restricted diet that is no help whatsoever, and, furthermore, suffering from serious psychological impairment because of the very nature of the diet. In older children and adults, it is much less likely that food sensitization is responsible for the skin lesions of atopic dermatitis. Dietary manipulations should be considered only in the more seriously involved patient, unresponsive to the well-known and accepted modalities of therapy. Inhalants Allergic reactions to inhalants, including sensitivity to pollens, dust, animal danders, and molds, have been implicated as a cause of atopic dermatitis. 4 When an inhalant allergen is suspected of aggravating the disease, the preferred method of tr~atment is, first, avoidance of the offending allergen. This is of particular importance and practical value in those cases in which there is intimate contact with animal danders of all kinds, including wool, cats, dogs, feathers, and parakeets, as well as excessive exposure to dust and molds. If avoidance or reduction of exposure is unattainable, as in the case of dust, molds, or pollens, and there appears to be a reasonable correlation between the clinical phenomenon and the skin tests, then hyposensitization therapy is indicated, particularly if the atopic dermatitis is of moderate or serious intensity. When resorting to hyposensitization therapy, meticulous cai-e is required, so that the dose of the specific extract will not exceed the limit of tolerance of the patient, for when this occurs, the atopic dermatitis is apt to be made worse. There is, however, another reasonable and practical aspect of reducing or avoiding contact with inhalant allergens, and that is that continuous exposure to and contact with potent inhalant allergens may lead to future sensitization and be partly or wholly responsible for the development of respiratory allergic syndromes, which are likely to occur in at least 40 per cent of all children affiicted with atopic dermatitis. Contactants Certain types of irritative garments, such as wool, can act as nonspecific irritants and perpetuate the inHammatory process of atopic
197
COMMON DERMATOLOGIC CONDITIONS
dermatitis. However, whether wool as such, acting against the skin, can, by specific sensitization, initiate the lesions of atopic dermatitis remains unanswered. Topical Therapy
Changes in the skin vary in the acute phase from mild erythema with scaling to oozing, with or without infection. In the chronic state, lichenification, with or without depigmentation, is prominent. Itching, which is the most profound and disturbing of all the symptoms, is generally more prominent after bedtime. Lack of sleep as well as general discomfort produces irritability, fretfulness, and loss of appetite. The usual signs and symptoms of infection may not be apparent when the patient is examined. Careful inspection for a solitary pustule, enlarged regional lymph nodes, or a history that the mother, or another child, is afflicted with a skin infection, may tell a good deal about infection in the patient. In mild cases, in which there is minimal erythema and scaling, simple measures usually suffice for suppressing the disorder. The most effective agents are the corticosteroid creams. For that matter, the single most important advance in the treatment of eczema during the past 20 years has been the advent and development of the corticosteroid hormones. Cort-Dome, Valis one, Synalar, or Kenalog, whose effects are enhanced considerably if the medicament is applied at least 10 times a day, is applied thinly and rubbed in vigorously to the affected areas. When there is improvement, the number of applications of corticosteroid cream is rapidly reduced. A modification of Rosen's ointment, which may be considered by some to be outmoded in the current steroid era, may be surprisingly helpful in many instances. This preparation is as follows: Burow's solution Polysorb Lassar's paste q.s. ad Sig.: Apply 4 to6 times a
10 20 60 day
For those patients whose lesions are oozing or weeping, nonirritating soaks with Burow's solution, prepared by dissolving one Domeboro tablet or powder in a pint of cool water, are carefully applied. Although any soft fabric may be used for applying a soak, an effective method is the use of cheesecloth. After a pack containing 20 layers or more of cheesecloth has been soaked in Burow's solution and placed over the affected area, a bath towel is wrapped around the moist dressings. A large sheet of plastic is placed under the child to protect the bedding and can, if desired, be used to hold the dressing in place. The pack should be kept moist and in place for as long as the child can tolerate it, which in most cases is not more than 20 minutes at one time. During the interval when
198
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the packs are removed, or during sleeping hours, Rosen's modified ointment or one of the various corticosteroid creams can be applied. Colloidal baths are soothing and anti-inflammatory and can be substituted twice or more a day for wet dressings. Laundry Linit, a commercial starch preparation, 2 cupfuls to a tub of water, is inexpensive and satisfactory, while Aveeno bath serves the same purpose. For lichenified lesions, tars with or without corticosteroid hormones are effective. For thickened lesions with associated infection, the quinolones are particularly useful. For chronic thickened lesions: Prescription 1: Liquor carbonis detergeris 1.80 Salicylic acid 3.00 Neobase q.s. ad 60.00 Sig.: Apply to affected areas 4 to 8 times a day Prescription 2: Cor-Tar-Quin 0.5% Sig.: Apply to affected areas 6 to 10 times a day Prescription 3: Vioform powder 1.80 Liquor carbonis detergens 1.80 Synalar (0.10%) 15.00 Lassar's paste i q.s. ad 60.00 Sig.: Apply to affected areas 6 to 10 times a day
Occlusive dressings may be utilized. Although the results are unpredictable and in some cases the eruption may even Hare, there is enough merit in this technique to deserve consideration as an important modality of therapy, particularly if the lesions are below the elbows and knees and are in the subacute or chronic stage. Any of the corticosteroid creams, such as Synalar, Cort-Dome, Kenalog, or Valisone, is applied sparingly to the lesions, rubbed in vigorously until the cream disappears, and then covered with a thin, pliable, noninflammable, transparent, moisture-retaining material, such as Saran Wrap or even a Baggie (small .. plastic bag.) When a plastic material is used, it is imperative that the bag be of such a small size as never to fit over a child's head, because of the danger of suffocation. For the hands, a plastic glove is ideal. When the open ends are sealed with 3 M Blenderm tape, an airtight compartment is provided, which prevents evaporation of moisture and in tum can promote rapid healing of the lesions. Occlusive dressings are applied at bedtime and removed in the morning. Localized infections are treated much the same way as an oozing wet lesion. Soaks with Burow's solution are used along with topical antibiotics, such as Bacitracin, Bacirnycin, Neopolycin, Neosporin, or Vioform. Dermatologic preparations that contain sulfa or penicillin are to be avoided, because sensitization reactions frequently result from their use. When there is evidence of spreading infection, or signs or symptoms of pustular or irnpetigenized areas, antibiotics, chosen by the results of
COMMON DERMATOLOGIC CONDITIONS
199
culture and sensitivity, are administered systemically along with wet dressings. Antihistamines Antipruritic therapy is essential for the management of atopic dermatitis. Although the antihistaminics are said to be potent antipruritic agents, control of pruritus using these medicaments is often less than satisfactory. It is also impossible to anticipate a patient's reactions to these drugs, because antihistaminics vary considerably in side effects and clinical response. Therefore the choice of an antihistaminic agent is usually made after experimenting with a number of preparations. The following antihistaminic agents may be used as directed, but the dosage may have to be lowered or increased according to the requirements and tolerance of the patient, or, because of ineffectiveness, another antihistaminie may have to be tried. Elixir of Benadryl or Phenergan Fortis are usually excellent choices for dispensing at bedtime, because they generally produce not only an antipruritic response, but also a strong sedative and, at times, a soporific effect. For a child aged 1 year, 3 teaspoons of Elixir of Benadryl, or Y2 teaspoon of Syrup of Phenergan Fortis, is offered. For the older child, Elixir of Benadryl may be increased to 4 teapsoons and Phenergan Fortis to 1 teaspoon. Anyone of the following can be prescribed as a daytime antihistaminic, in a dose of Y2 to 1 tablet, or teaspoon, three times a day: Chlor-Trimeton, Periactin, Actifed, Tacaryl, Dimetane, or Pyribenzamine. Aspirin, in the usual doses for children, is at times an effective antipruritic agent which can be taken alone or along with an antihistaminic. Other Medications Tranquilizing agents are occasionally beneficial in the treatment of atopic dermatitis, because they relax the patient and thus reduce pruritus and scratching. Some tranquilizing agents are even more helpful because of additional antihistaminic effect. An example of this is Syrup of Atarax, which is offered in a dose of 1 to 2 teaspoons three times a day. As a substitute for an antihistaminic, and particularly when sedation is desirable, chloral hydrate may be dispensed as Noctec, 1 to 2 teaspoons, at bedtime. Noctec contains 7.5 grains of chloral hydrate per teaspoon. Unfortunately, the response to phenobarbital has been extremely disappointing, because its actions are unpredictable; more often than not, the child is stimulated. It is suggested that soaps of all kinds be avoided during the acute phase of atopic dermatitis. However, pHisoHex is particularly useful in the acute stage and also if the skin is infected. Nonallergenic soaps, such as Aveeno-Bar, Lowila Cake, or Neutragena, all of which are nonkeratolytic and have a pH that approximates that of the skin, are suggested for subacute or chronic stages of atopic dermatitis.
200
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BERMAN
For softening dry skin, which may be responsible for pruritus and scratching, applications of specific medicaments are recommended. Examples of skin softeners are Alpha Keri, Domol, and Ar-Ex Bath Oil, all of which require 2 capfuls to a tub of water. Also of value are various skin softeners, which are applied after a bath. Effective and cosmetically acceptable are Keri Lotion, Ar-Ex Body Lotion, and Allercreme Special Formulated Skin Lotion. Unfortunately, with the availability of topical corticosteroid hormones, which have simplified the treatment of this disorder, there has been a tendency to neglect other equally important areas of therapy. For example, when there is extensive skin involvement, particularly involving the extremities, a practical measure is to apply a loose white cotton covering, or a bandage, enclosing the affected area. This serves to protect the skin from irritants, such as garments or rugs, which through frictional contact increase itching and aggravate lesions. Furthermore, maceration of the skin by an infant who crawls on rugs or floors can be minimized by such a simple protective covering. Corticosteroid Honnones Systemic corticosteroid hormone therapy may be needed as shortterm treatment for severe disseminated atopic dermatitis. Although no one particular cortisone derivative is more effective than any other, prednisone, because it is less expensive, is usually prescribed, in a dose of 30 to 50 mg. for the first 24 to 48 hours. At th6l end of this time, if there is improvement, the prednisone is gradually reduced, so that no more is given by the seventh day. The corticosteroid hormones are prescribed along with all the other modalities of topical therapy. If the patient is no better, then hospitalization may be necessary. Needless use of systemic corticosteroid hormones is contraindicated, particularly when other avenues of treatment will suffice for control of the disorder. Furthermore, long-term daily use of suppressive doses of corticosteroid hormones is ill-advised, because of the well~Imown sequelae and complications. However, there are instances of hard-core intractable eczema, and long-term steroid therapy can, by judicious use, convert a totally disabled child, both physically and emotionally, to one who is able to be comfortable, to sleep well, feel well, and participate in normal school and play activities. If there is a need for continuous steroids, then the alternate day administration of corticosteroid hormones, if effective, is the treatment of choice. Side effects from alternate day steroids are minimal; the child usually grows normally, and adrenal function is not appreciably altered. Because of their characteristic rate of excretion, dexamethasone, triamcinolone, and betamethasone are not suitable for alternate day administration. Used in this manner, these agents quickly produce signs and symptoms of steroid overdosage. I have observed that prednisone is the most satisfactory corticosteroid for alternate day therapy. The drug is administered initially in higher
COMMON DERMATOLOGIC CONDITIONS
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dosage, reduced quickly as the rash improves, and continued as a single dose, after breakfast, every other day. In some instances, children have been made comfortable with as little as 5 to 10 mg. of prednisone, while a few patients have required as much as 20 to 25 mg. for adequate control. With careful patient selection, with an appreciation of side effects, and exercising sound judgment for prompt withdrawal when no longer needed, corticosteroid hormones, whether used for short-course daily treatment or for longer-term alternate day administration, are important additions in the care of atopic dermatitis. Instructions for the care of a small child with atopic dermatitis are as reproduced as Table 4. Table 4.
Sample Instruction Sheetjor Home Care oj an 18-Month-Old Child with Atopic Dermatitis
Please follow these instructions carefully; the directions given under Plan A are to be followed daily. The vaporizer need not run all day-only when the child is put to bed at night. Be sure to add sufficient water that the vaporizer will be effective during the time that the child is sleeping. If the eruption flares, in addition to continuing with all the items in Plan A, go to Plan B. Apply cream No.1 thinly and evenly and rub it in vigorously. If the eruption is intensified or appears more irritated after application of the cream, stop applying it promptly and call this office immediately. As soon as the rash has improved dramatically, diminish the frequency of application to once or twice a day. If there are signs or symptoms of infection, a matter we have previously discussed with you, use cream No.2 in place of cream No. 1. The directions for the use of cream No.2 are the same as for cream No. 1. If eczema involves the hands or feet, try Plan C. If the symptoms appear to be worse, discontinue Plan C promptly. If, after following these instructions, the patient's skin is no better, please call the office for further instructions. Plan A: Care of the Skin Neutragena (substitute for soap) Alpha Keri, 2 capfuls to a tub of water Cold mist vaporizer Elixir of Benadryl, 1 tablespoonful at bedtime ChI or-Trimeton, ~ teaspoonful morning and noon Allercreme Special Formulated Skin Lotion, after bath as a skin softener Plan B: If the Eruption Flares Cream No.1: Cort-Dome Cream, ~% .. Apply 10 times daily thinly to affected area and rub in vigorously. Cream No.2: Neo-Cort-Dome Cream, ~%. Apply 10 times daily thinly to affected area. Plan C: For Rash of Hands or Feet Cort-Dome Cream is spread thinly and rubbed in vigorously over the affected area. Saran Wrap .covers the lesions to form an airtight compartment. The ends are sealed with Blenderm, a nonallergenic tape. The Saran Wrap is applied at bedtime and removed in the morning.
Humidification Serious harm to the mucous membranes of the respiratory tract, as well as the skin, can result from excessively dry air. This problem is especially troublesome and common in temperate climates, usually in the winter months and in those homes where central heating is required
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continuously for many months each year. Most homes in cold weather have relative humidities ranging from 10 to 15 per cent, probably with lesser percentages recorded where the heating is through duct systems. Ideally, a relative humidity of 30 to 40 per cent is recommended, but this is often unattainable even with central humidifiers in those sections of the country where temperatures outside the home rarely rise above 10° F. Dry heated air acts as a sponge, soaking up moisture and drying the skin and mucous membranes of the respiratory tract, and is particularly injurious to those patients afHicted with atopic dermatitis or respiratory allergic disorders. Excessive dryness of the skin frequently is responsible for pruritus, even without the presence of atopic lesions. Therefore adequate humidity in the home is a prerequisite for the proper care of the child with atopic dermatitis, for, by its effect of keeping the skin moist and soft, pruritus may be markedly lessened. An important byproduct of sufficient moisture in the air is that it reduces brittleness of various fabrics in the home, thus lessening dust and lint formation. Cool mist humidifiers range in size from small, inexpensive room appliances to more sophisticated and expensive central humidifiers, for which one must have a duct system. For the single room the Hankscraft or similar DeVilbiss apparatus is practical. For humidification of larger areas of the home and where there is no duct system available, a larger console humidifier is practical. Examples of this type are Arvin, Walton, and Sunbeam. Immunization Most physicians are aware of the untoward and serious effects .of herpes simplex and vaccinia virus. In patients with atopic dermatitis, both can produce the syndrome of Kaposi's varicelliform eruption. Apparently, atopic dermatitis lowers the host's resistance to these viruses. For those whose eruption is caused by the vaccinia virus, there is available a specific vaccinia-immune gamma globulin preparation, which, when administered in proper dosage! (1 ml. per kg. of body 'weight) can be extremely effective and, at times, life-saving. In the presence. of atopic dermatitis, vaccination of the patient or other members of the family is contraindicated, and close contact with other vaccinated children is forbidden. SEBORRHEIC DERMATITIS
Seborrheic dermatitis, the most commonly encountered dermatitis of infancy, is a disorder of unknown origin, most often a benign, self-limited eruption, but at times chronic and often confused with and misdiagnosed as atopic dermatitis. Seborrheic dermatitis is characterized by two principal forms. One is a scaly eruption (scales may be dry or greasy) on an inflammatory base, affecting chiefly the scalp, eyebrows, eyelids, upper
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portion of the face, pubic regions, and presternal areas of the trunk. Another form, intertriginous, is usually moist and involves the postauricular, axillary, and inguinal areas, as well as other flexural areas. Table 5.
Differential Diagnosis Between Atopic Dermatitis and Seborrheic Dermatitis* ATOPIC DERMATITIS
Family history of allergy Skin tests Pruritus Eosinophilia Association with respiratory allergies General distribution
Usually positive
Not so commonly positive
Positive reaction to foods and inhalant allergens Always present
Usually negative
Nasal and blood eosinophilia are common %: of all patients The face, flexor surfaces of the upper and lower extremities, dorsal surfaces of the arms and legs
Color, shape, and nature of eruption
Scales are white, usually not large, and the edges rarely curl; serpiginous outlines are rare; erythema, scaling, oozing, crusting, and secondary infection, as well as lichenification, are common
Scratch marks Secondary infection Depigmentation Flexor involvement
Very common Common Common Lichenification prominent in chronic lesions; creases of flexural surfaces of arms are involved, and the process frequently extends up and down the forearm quite a distance; the same distribution is frequently noted on the lower extremities Lesions mayor may not be present
Scalp
Injection therapy Elimination diet Prognosis
* From 1956.
SEBORRHEIC DERMATITIS
Glaser,
Sometimes helpful Sometimes useful Guarded
J.
May be present, but is rarely as severe as atopic dermatitis Rarely present Less than
~
of all patients
Chiefly the scalp, eyebrows, eyelids, along the hairline, and upper portion ofthe face; occasionally cheeks, pubic region, and presternal area of the chest; intertriginous involvement of the posterior auricular, axillary, and inguinal areas Body lesions are often in the shape of waxy plaques that appear yellow when the skin is tensed; frequent greasy scales, "potato chip" in appearance, with edges that curl; coalescent large lesions with serpiginous borders; moist lesions in intertriginous areas Rare Rare Does not occur No lichenification; flexor lesions are confined to the skin surfaces that touch one another; for that matter, the eruption typically occurs wherever the skin surfaces come together, e.g., in fat folds of the abdomen and elsewhere Typical cradle cap always due to seborrheic dermatitis, never atopic dermatitis Not needed Never useful Practically always good
G.: Allergy in Childhood. Springfield, Ill., Charles C Thomas,
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It has been suggested that seborrheic dennatitis is a forerunner of atopic disease, because a small percentage of patients with seborrheic dennatitis will gradually develop the skin eruption consistent with a diagnosis of atopic dennatitis. Also, the two disorders frequently coexist. Prompt treatment of seborrheic dennatitis will not prevent the development of atopic dennatitis. Because there are many infants with seborrheic dennatitis who never develop atopic dennatitis, it is important to make an accurate differential diagnosis between these two disorders (Table 5). As a rule, the patient with seborrheic dermatitis has little or no pruritic involvement, has negative skin tests, and rarely develops subsequent respiratory allergic diseases. Therefore there is no reason for skin tests, elimination diets, or hyposensitization therapy, nor a need to induce anxiety in parents who dread the diagnosis of atopic dennatitis.
Treatment For seborrheic involvement of the scalp, a variety of shampoos are available and are usually effective. All these preparations are potential irritants and should be discontinued promptly if undue skin irritation is present. The hair is shampooed at least twice a week. Any of the following may be used as a shampoo and the directions are the same for all: Fostex Cream, Sebutone, or Sebulex. Massage a liberal amount of the preparation into the wet scalp for 3 to 5 minutes, rinse, repeat, then rinse thoroughly once again. After shampooing, apply one of the following at least twice a day: Neo-Synalar, Cordran-N, Synalar Solution, Kenalog-N, or Neo-Cort-Dome. For stubborn cases involving the scalp, one can turn to some of the older and established therapeutic preparations, which may help. The following is an! example: Salicylic acid 1.80 Sulfur ppt ..• 2.00 Neo Base q.s. ad 60.00 Sig.: Rub into the scalp 2 or 3 times a week at night and wash out the next day
Pragmatar or Packer Tar Shampoo is also useful. If these medicaments prove ineffective for removing thickened scalp lesions, then an occlusive technique may be surprisingly helpful. After applying a tar shampoo and rinsing thoroughly, one of the aforementioned corticosteroid creams is rubbed in liberally and vigorously, covered by Saran Wrap, and kept in place by a shower cap tied loosely under the chin. The occlusive dressing is applied at bedtime and removed in the morning. This procedure, which may have to be repeated several times before there is improvement, is not suitable for infants or young children because of the potential hazards of plastic material near the face.
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For lesions of the body, Vioform ointment, Vioform hydrocortisone, Cordran-N, Kenalog-N, Neo-Cort-Dome, and Neo-Synalar are all excellent preparations. For marginal blepharitis, believed to be of seborrheic origin, 10 per cent sodium sulamyd ointment is useful. Erythroderma desquamativum (Leiner's disease) is a generalized and intensified form of seborrheic dermatitis. Treatment is the same as for the milder forms of seborrheic dermatitis. If topical steroids need to be used, but are of no help, then a short course of oral corticosteroids may have to be utilized. Petrolatum, with or without salicylic acid, 5 grains to the ounce, is often of some help. pHisoHex is useful to reduce secondary infection. These babies can run a stormy course, so that hospitalization is frequently necessary. Severe gastrointestinal disturbances, particularly diarrhea, are cardinal features of this disorder. Correction of dehydration, maintenance of adequate nutritional intake, and control of diarrhea and infection are best accomplished in a hospital setting. In this country, unlike Europe, this disease is rare. Its duration is usually not over 3 months, recovery is permanent, and there are no sequelae.
CONTACT DERMATITIS
Contact dermatitis, a common and troublesome disorder, is mediated by a delayed hypersensitivity reaction. The diagnosis is suspected by history, morphology, and distribution. A multitude of different sensitizing agents can be responsible for the eruption, including chemicals, jewelry, drugs, cosmetics, and plastics. The list is limitless and, of course, must include members of the plant kingdom. By far the most common contact allergic eruption from plants is caused by poison ivy, poison oak, or poison sumac, all included under the generic botanical term Rhus. It is important for the physician to realize that not all plant dermatitis is caused by poison ivy or its biologically related plants. Although less frequently involved as causative factors, the following can induce contact dermatitis: primrose, chrysanthemum, ragweed, a variety of trees and grasses, as well as large numbers of fruits and vegetables. When sensitization is established, the changes in the skin may range from mild erythema with scaling to vesiculation, oozing, bullae, and even lichenification. Pruritus is usually intense. Patch tests are typically positive, while scratch and intradermal tests are almost always negative. The symptomatic treatment of contact dermatitis is essentially the same as for atopic dermatitis. Poison Ivy (Rhus toxicodendron) A few additional comments regarding poison ivy are essential. The sensitizing factor, an oleoresin, is contained in the sap of the leaves.
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Contact is made either by touching the plant, by standing nearby when the leaves are being burned, or by patting a dog or cat that carries the active sensitizing fraction-or even by handling contaminated garments, logs, or other plants. Characteristically, several days after contact with the sensitizing fraction, the patient develops vesiculation, erythema, marked edema, oozing, and moderate to severe pruritus. Vesicles are often distributed in linear fashion. The exposed areas of the body are quick to develop eruptions, followed in a few days, in some instances, by involvement of other remote skin areas. It is important to remember that the serous exudate from the lesions does not contain the active sensitizing fraction, and represents only the inHammatory response of the host to poison ivy. Because the oleoresin of poison ivy is gluelike, it can remain fixed to the skin, still capable of sensitizing, for several days or longer. Therefore it is advisable that unaffected areas of the skin be scrubbed vigorously and involved sites washed gently with soap and water. All clothes suspected of being contaminated should also be cleansed thoroughly. For local and minimal involvement of the skin, soaks, orally administered antihistaminic agents, and topical corticosteroid creams are sufficient. For the patient with intense local or generalized poison ivy dermatitis, or for that matter severe contact dermatitis from other causes, orally administered corticosteroids are the treatment of choice. Calamine lotion and liniment are of little or no help. Tap water soaks and optimum doses of antihistaminics, administered along with corticosteroid hormones, will lessen the intensity of the eruption in about 48 hours. Prednisone, 2 mg. per kg. per 24 hours, is the preferred corticosteroid preparation. However, satisfactory results will usually follow if prednisone is administered in a dose of 50 mg. on the first few days and then, as improvements follows, is rapidly reduced, so that no more is given by the seventh or eighth day. Attempts have been made to prevent poison ivy sensitivity (as well as that of poison oak and poison sumac) by injection of alum-precipated pyridine extracts of poison ivy (Dome Chemical Co.) given well in advance of the season. Others have resorted to oral preparations of a poison ivy extract (Hollister-Stier Laboratories, Inc.) to provide protection. Beneficial results from the use of these products have been reported. Others refer to their placebo effect, describing them as worthless. Ii In any event, if hyposensitization is contemplated, it should be utilized only for the most sensitive patients, specifically those who have serious eruptions year after year, despite all attempts to avoid contact with the plants. These preparations are not without side effects. They should be discontinued promptly, then restarted at lower dosage, if dermatitis or pruritus ani (not uncommon with oral extracts of poison ivy) are observed, and they should never be administered in the presence of clinically apparent poison ivy.
COMMON DERMATOLOGIC CONDITIONS
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URTICARIA
Urticaria, a common a:ffiiction, is characterized by localized or generalized crops of wheals, usually evanescent, associated with itching and burning and sometimes involving mucous membranes of the respiratory and gastrointestinal tracts. Urticaria (or hives) results from the influence of one or more chemical mediators upon the capillaries or venules. If the individual urticarial lesion is extensive and marked by intense edema, it is termed angioedema. Not all urticaria is allergic. When allergenic factors are involved, the condition usually results from a reaction of the specific allergen with its corresponding antibody, which releases one or more chemical mediators, which in tum act on the capillary bed. Nonallergenic causes are equally important in the development of hives, which may be present as an acute self-limited disorder, or a chronic relapsing condition. The patient is said to have chronic urticaria when the process has been present for weeks (usually 4) to months. Chronic urticaria, occurring far less often in children than in adults, is often difficult to manage. Determining the cause of hives is frequently a tedious and complex procedure. Table 6 is an oversimplified chart demonstrating the multitudinous origins of this disorder. In children, hives generally occur as an acute, self-limited process, and often cannot be related to anyone causative factor. When a cause can be isolated, the most likely ones are acute infection, drug allergy, ingestion of a specific food, or inhalant allergy to pollens, animal danders, or miscellaneous allergens. In children, chronic hives involving the extreInities should raise a suspicion of papular urticaria; when hives are linear, dermographism is the most likely explanation. Sensitivity to foods should be given serious consideration when caring for a patient with chronic urticaria. In most instances, scatch or intradermal tests for foods are of little or no help in identifying the responsible allergens. If skin tests are negative, elimination diets, coupled with food diaries, are the choice of management. For a complete discussion of the technique of administration of elimination diets, the reader is referred to the section on "Atopic Dermatitis." The· offending foods are many, but it is generally agreed that milk, eggs, pork, chocolate, nuts, fish, shellfish, and fruits are the most common offenders. Reproducible evidence of hives occurs within seconds to several days after the ingestion of the offending food. Drug-induced urticaria is complicated by the fact that the patient or parent often does not volunteer or admit to taking drugs unless specifically questioned. There is no intentional withholding of information, but many do not appreciate or consider that cathartics, tranquilizers, weight-reducing agents, and aspirin fall into the category of drugs.
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Table 6.
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Etiology oj Hives
1. Ingestion of specific foods, coloring agents or fillers in foods, such as nuts, chocolate, fish, lobster. 2. Inhalant allergens: animal danders, including dogs and cats, or pollen urticaria, often called seasonal hives, caused by exposure and sensitivity to the various pollens of trees, grasses, and weeds. 3. Drug allergy, including all drugs. Most common, however, is penicillin (even the traces of penicillin found in cow's milk as a result of treating infected udders with this drug). 4. Papular urticaria-common on the extremities and thought to be due to sensitivity to bites of bedbugs, fleas, mites, or mosquitoes. Lesions are both papular and urticarial, are intensely pruritic, and often are infected because of scratching. 5. Hymenoptera sting-systemic reaction resulting from the bite of a bee, wasp, yellow jacket, or hornet (there is a similar reaction from an ant bite, but this occurs rarely). Prevention of recurrence of systemic reaction is essential and is accomplished, in most instances, by injection therapy with extracts containing equal parts of b("e, wasp, yellow jacket, and hornet. Hyposensitization continues for 3 years or longer. 6. As a consequence of injection therapy for the treatment of inhalant allergies-overdose of pollen produces systemic reaction, associated in part with urticaria. 7. Injection of antisera (horse serum), such as tetanus antitoxin; when fever and swelling of the joints are also present, the process is called serum sickness. 8. Infection, acute or chronic (viral or bacterial). 9. Parasitic infestation. 10. Cholinergic urticaria, following exposure to heat, exercise, or emotion and sometimes reproducible by injection of cholinergic drugs. Lesions are pea-sized and discrete. 11. Urticaria occurring after contact with water of any temperature; even noted with patient's own sweat. 12. Physical factors, including cold, heat, and light. There is some evidence that physical allergy may be mediated on an immune basis, because in some cases the process may be passively transferred. 13. Hereditary angioneurotic edema. Laryngeal edema is common and accounts for the high mortality in this disorder. These patients lack serum inhibitors of an enzyme derived from the first part of complement. 14. Agents or drugs that release bound histamine, including morphine, codeine, certain toxins, and venoms (snake bites). 15. Dermographism. Reaction caused by gentle stroking of the skin. Usually produces whealing in linear form. Frequently confused with hives of immune origin. 16. Urticaria pigmentosa. Patients have, scattered over the trunk, isolated or multiple brown or yellowish brown macules about 1 cm. or larger in diameter. Rubbing the lesions produces localized urticaria (Darier's sign). The lesions on the skin are conglomerates of mast cells which release histamine when traumatized. Similar clusters of mast cells may occur in other organs. 17. Urticaria associated with morbid systemic diseases: lymphoma, leukemia, and systemic lupus erythematosus. 18. Urticaria caused by endocrine disorders-pregnancy; menses; thyroid disease. 19. Emotionally induced urticaria.
Therefore, in history taking, it is important to elicit each of the medicaments ingested by the patient. It is not sufficient to ask the patient, "Are you taking any drugs?" Physical causes of hives are the subject of renewed interest. Cold urticaria is of particular concern because of possible accidental death occurring under certain circumstances. Swimming in cold ocean water induces urticaria, and if the precess becomes intense and generalized, syncope and drowning may occur.
COMMON DERMATOLOGIC CONDITIONS
209
The most effective management of urticaria, whether acute or chronic, depends in a large measure on finding the cause-which, however, is not always possible. Symptomatic treatment relies chiefly on the various antihistaminic preparations. In my experience, Atarax has been the most consistently effective preparation. The dose of Atarax should be pushed to tolerance, or control of symptoms, whichever occurs first. In a few instances, as much as 50 to 100 mg. three times a day is required to suppress the eruption. For disseminated urticaria, either acute or chronic, and unrelieved by optimum doses of antihistaminic preparations, injectible agents, such as epinephrine or Benadryl (1 mg. per kg., not to exceed 40 mg. per single dose) administered subcutaneously, may help. Short courses of corticosteroid hormones may be needed for severe cases. When there is laryngeal edema, prompt and vigorous treatment with subcutaneous epinephrine, or even tracheostomy, is necessary. Injection therapy with appropriate allergens may help if pollens or miscellaneous allergens, such as dust or molds, are the responsible agents. When hives result from drug or food ingestion, or exposure to animal danders, and the specific causative factor can be uncovered and removed, improvement is likely to occur.
ACKNOWLEDGMENT
The author wishes to thank Dr. Jerome Glaser of Rochester, New York, for permission to use material from his book.
REFERENCES 1. Gellis, S., and Kagan, B., eds.: Current Pediatric Therapy III. Philadelphia, W. B. Saunders Co., 1968. 2. Glaser, J. G.: Allergy in Childhood. Springfield, Ill., Charles C Thomas, 1956. 3. Glaser, J. G.: The prophylaxis of allergic disease in infancy and childhood. Acta Paediat., 46:43, 1957. 4. Hill, L. W.: The Treatment of Eczema in Infants and Children. St. Louis, C. V. Mosby Co., 1956. 5. Kanof, N. B., and Baer, R. L.: Attempts to hyposensitize with poison ivy extracts. Ann. Allergy, 22: 161, 1964. 6. Rostenberg, A., Jr.: Atopic dermatitis: A discussion of certain theories concerning its pathogenesis. In Baer, R. L., ed.: Atopic Dermatitis. New York, New York University Press, 1955, p. 65. 7. Stifler, W. C., Jr.: Conference on infantile eczema. J. Pediat., 66:235, 1965.
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