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Contact Dermatitis in Children
Symposium on Pediatric Dermatology
Contact Dermatitis in Children
Ernst Epstein, M.D. *
A chemical can cause contact dermatitis by two fundamentally different mechanisms - irritancy and allergy. 7 , 10 Irritant dermatitis, usually called primary irritant dermatitis, results from nonspecific skin injury. Acids, strong alkalies, and detergents are examples of irritants capable of causing primary irritant dermatitis by a nonspecific skininjuring effect. The allergic type of contact dermatitis depends on the existence of a specific antibody. The patient will not react with allergic contact dermatitis unless allergy, an acquired specific alteration in the capacity to react, exists. Poison ivy and poison oak are common causes of allergic contact dermatitis in North America. Generally when dermatologists refer to contact dermatitis they mean allergic contact dermatitis. Allergic contact dermatitis is clinically the more significant type of contact dermatitis, and this discussion will be limited to it. For brevity we will use the phrase "contact dermatitis" to mean "allergic contact dermatitis."
FUNDAMENT AL ASPECTS Allergic contact dermatitis is a true allergic process resulting from an antibody-antigen reaction. The antibody responsible for allergic contact dermatitis is fixed to cells of the lymphoid system. This type of fixed antibody produces a reaction only after a delay of hours or days after contact with the antigen. Hence this type of allergy is referred to as delayed, or "contact type," allergy. Because the antibodies are fixed to cells, serologic tests are of no value, and it is necessary to apply the allergen to living tissue to detect the presence of antibody. Delayed allergy is responsible for the tuberculin test in which the antigen (tuberculin) is either injected into the skin (Mantoux test) or applied to the skin (Vollmer's test) as a patch test. After a delay of 48 to 72 hours, a reaction is apparent if allergy exists. While both the intradermal and patch tests are theoretically suitable for detecting contact type allergy, "'Clinical Assistant Professor of Dermatology, University of California, San Francisco Medical Center
Pediatric Clinics of NorthAm erica- VoL 18, No.3, August 1971
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in the investigation of contact dermatitis only the patch test method is practicaL" Delayed or contact type allergy is, like other allergies,· acquired. Sensitization is a complex process, depending both on exposure and the innate ability to become sensitized. Much work has been done on experimental sensitization, and ways of preventing it. In animals, and apparently in man, it is possible to prevent or minimize sensitization by suitable pretreatment with the allergen. l l There has been much debate whether patients with certain dermatologic disorders, particularly atopic eczema, are more prone to develop contact sensitization than normal individuals. It has been clearly demonstrated that inflamed or dermatitic skin is more prone to sensitization than intact skin. However, it appears that patients with atopic dermatitis are no more prone to develop contact allergy than patients with eczematous dermatoses of other etiology.2 Delayed or contact type allergy is fundamentally different from immediate or anaphylactic sensitiv:ity. In immediate allergy we are dealing with a circulating antibody which produces a whealing reaction within minutes after scratch or intradermal testing. Urticaria and anaphylaxis are reactions caused when immediate type antibody reacts with antigen. The immediate type of allergy has nothing to do with contact dermatitis, and scratch and intradermal testing for immediate type allergy are of no value in the diagnosis of contact dermatitis. Atopic dermatitis and contact dermatitis are sometimes confused. These are two distinct and unrelated entities, which may co-exist. Atopic dermatitis (also called constitutional eczema) is an inborn defect, the nature of which is unknown. Atopic dermatitis is not an allergic disease, although it is often, and incorrectly, referred to as "allergic eczema" or "skin allergy." The patient with atopic eczema characteristically has dry skin, abnormalities in reactivity of the skin vasculature, sensitivity to irritants such as rough clothing, as well as circulating antibodies of the immediate whealing type to a variable number of substances. The relationship of the atopic antibodies, or reagins, to the patient's eczema is in most cases uncertain. It is clear that nonspecific measures such as topical steroids, skin lubrication, and avoiding irritants are far more successful in controlling atopic dermatitis than desensitization or elimination techniques directed toward atopic allergens discovered by scratch and intradermal testing. Another area of confusion is the meaning of the word eczema. Eczema is a morphologic term describing a reaction pattern, and is not a diagnosis. Dermatologists use the word eczema to describe a nonspecific inflammatory reaction of the skin manifesting erythema, scaling and varying degrees of exudative change. Unfortunately some physicians consider the term eczema as synonymous with atopic dermatitis. Using the word eczema to mean atopic dermatitis is both incorrect and con*Intradermal testing for contact allergy can be performed with certain allergens which are water soluble and non-irritating under test conditions. However" in contact dermatitis, the intradermal test is generally a research tool.
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fusing, since eczema may result from many processes besides the atopic state. Eczema remains a very useful term to describe a cutaneous reaction pattern. Eczema and dermatitis have essentially the same meaning, British authors usually preferring dermatitis.
DIAGNOSIS The diagnosis of allergic contact dermatitis is based essentially on the history and physical findings, particularly the distribution of the eruption. The patch test is the only test available for the investigation of contact dermatitis. The patch test is tricky, both in execution and interpretation, and is best left to experts. Fortunately, when contact dermatitis occurs in children, patch testing is usually not necessary. Often the diagnosis of allergic contact dermatitis is evident at once-for example, a patchy, streaky vesicular contact dermatitis in a youngster who has been in the woods of California is almost certainly caused by poison oak. On the other hand, the diagnosis may be exceedingly difficult, as when allergy to a topically applied medicament complicates a pre-existing dermatitis such as atopic eczema. In complicated situations, a high degree of clinical suspicion combined with shrewd observations and careful patch testing is necessary to sort out the complex events occurring in the skin. There are two aspects to making a diagnosis of contact dermatitis: (1) Is the dermatitis a contact dermatitis, and (2) if so, what is the contactant responsible? In the differential diagnosis of contact dermatitis, the distribution and patterning of the lesions is often of more help than the morphology of the lesion itself. Contact dermatitis is often an eczematous process, the individual patches of which may be quite indistinguishable from eczematous dermatitis of endogenous cause such as atopic or seborrheic dermatitis. When extensive, it may be difficult to distinguish contact dermatitis from a drug eruption. Furthermore, there is no consistent way of judging, from the appearance, whether a dermatitis is an allergic contact dermatitis or the result of nonspecific skin irritation. The distribution and patterning of allergic contact dermatitis frequently provides useful clues. For example, plants of the Rhus (poison ivy, poison oak) usually produce a streaky, patchy, very acute dermatitis on exposed areas. The history may be very important in the diagnosis of contact dermatitis; it usually must be a directed history, following up leads suggested by the clinical appearance of the eruption. If a plant contact dermatitis is suspected, questioning as to contact with brush, pets who have roamed in the woods, etc., is indicated. On the other hand, if one suspects a topical medicament, intensive inquiry as to self-treatment and previous medical therapy with topicals is necessary. Sometimes considerable skill and a great deal of persistence are needed to ferret out the answer. It should be emphasized that in this situation, examination and history complement and supplement each other, and repeated attempts are often necessary to elicit the significant information.
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Most physicians treating children tend to overdiagnose contact dermatitis. All too often a patch of atopic eczema. a persisting diaper dermatitis, or skin that has become irritated from excessive soap and water scrubbing is labeled as contact dermatitis. Except for acute plant contact dermatitis to the Rhus family, allergic contact dermatitis is not common in children. Most eczematous dermatoses of children are the result of endogenous factors (atopic or seborrheic) combined with nonspecific irritant effects of soap, water, rough clothing, etc.
PATCH TESTING Patch testing is of great value when investigating an obscure case of suspected contact dermatitis. 7 ,lO In principle, the test is simple; the suspected agent is applied to the skin under an occlusive dressing for 48 hours. Inflammation at the test site indicates allergy. While the principle of the patch test is simple, in practice it is quite complex. 1 Not only does the result of patch testing differ with the skin site and test covering used,12,13 to further complicate matters, false-negative and false-positive test results may occur. Many commonly used substances which do not irritate in ordinary usage, such as tincture of Zephiran, or shampoos, may cause nonspecific false-positive irritant reactions under the conditions of the patch test. On the other hand, certain substances such as neomycin will give false-negative patch tests in patients allergic to them. When the usual commercial ointment containing 0.5 per cent neomycin is used in the patch test, at least 50 per cent of patients with proven neomycin allergy will have a negative test. 4 One of the reasons for false-negative results is that patch testing must be done on intact skin, which is less reactive than the inflamed skin to which the topical medicament is applied. In the case of neomycin, the correct patch test concentration is 20 per cent! The complexities and pitfalls of patch testing are well discussed by Fisher 7 and by Hjorth and Fregert. 10 Patch testing is best left to those with experience with this tricky biological test.
PHOTO CONTACT DERMATITIS A fascinating variant of allergic contact dermatitis is photo contact dermatitis. In this situation, an agent sensitizes the skin surface to sunlight. Dermatitis from contact with the photosensitizing allergen occurs only in the presence of sufficient light. The compounds causing a photo contact dermatitis are essentially limited to certain topical antiseptics such as the brominated salicylanilides added to some of the antiseptic soaps. In my experience, photo contact dermatitis in children is rare. In photo contact dermatitis ordinary patch tests may be negative. It is usually necessary to have the patch test site exposed to suitable light after removal of the patch test, and to read the test result 24 hours after the light exposure. 6 , 9
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CAUSES OF CO TACT DERMATITIS In children the mo t common cau es of contact dermatiti encountered in orthern California are plant (poi on oak), topical medicamen t , hoe , n ic kel, and cosmetic . Plants In orthern California, the va t majority of ca e of contact dermatitis in children are caused by the plant of the Rhu family known as poi on oak (Fig. 1). Any patient allergic to one member of the Rhu family (poi on oak, poison ivy, poison sumac) i allergic to the other . Furthermore , the aller ic component of mangoe and the Japane e lacqu er tree cro -reac t with the Rhu allergen. In many patient with acute poi on oak con ta c t dermatiti the diagnosi i ea y and in fact ha u ually been m ad e b the patient. Exposure to bru h , followed by treak and patche of a cu te dermatiti , i practically diagno tic. Howe er, wh n contact with the plant i indirect uch a from a pet that h a roamed the wood , the dermatiti tend to be more diffuse and the diagno i may be difficult unle uch indirect ource of expo ure are u pected. U ually poi on oak con ta ct dermatiti appear 1 to 3 day after expo ure. Howe er, in tho e patient pre iou ly not allergic to poi on oak who become ensiti zed a a re ult of their exposure, the eruption appear only after a latent period of 9 to 14 day or more. The pattern of dermatiti in the e patient where the exposure is both en iti.zin.q and elic it in g tend to be different than in tho e patient with e tabli hed allergy. In tead of rapid de elopment of the dermatiti there tend to be a low increa e in e erity of the dermatiti a the patient' fixed antibodie increa e. Because of the more prolonged cour e of the dermatitis , longer period of y temic corticoteroid therapy are often required to control the dermatiti .
Figure 1. c u te pla n t co n tac t dermat iti from poi on oak wit h c harac teri tic tr ea k and patc he of ve icula r de rm at iti ( ee a l 0 color plate IIIB ).
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In areas where ragweed abounds, ragweed may cause a stubborn, chronic, but definitely seasonal contact dermatitis frequently incorrectly diagnosed as endogenous eczema (neurodermatitis). This is uncommon in children. The offending agent is a fat soluble oily fraction of the ragweed plant quite distinct from the allergen causing hay fever and asthma which are caused by a water soluble protein fraction of the ragweed plant.
Topical Medicaments These are probably the next most common cause of contact dermatitis in children. It is difficult to make firm statements as to which topical medicaments are the most common offenders since this depends both on the pattern of usage, and the sensitizing capacity of the medicament. 3 For example, penicillin applied topically is a very potent sensitizer; yet we do not see contact dermatitis from penicillin since penicillin ointments were withdrawn from usage years ago. Currently in Northern California, neomycin, ethylenediamine, and thimerosal (Merthiolate) are the most common troublemakers. Neomycin allergy is frequently hard to diagnose since it often produces only a chronic aggravation of the underlying skin disorder and is suspected by neither patient nor physician (Figs. 2, 3, 4). EthylenediaInine is an excipient found in only one medicament, Mycolog cream. Mycolog cream also contains neomycin, a second potent sensitizer. Thimerosal (Merthiolate) produces its share of dermatitis because patients are fond of painting it on their rashes. Although thimerosal contains mercury, patients allergic to thimerosal are sensitive to the organic part of the molecule and not to mercury. On the other hand, patients allergic to merbroInin (Mercurochrome) are allergic to mercury. Mercury allergy is still an occasional problem, as ammoniated mercury, yellow oxide of mercury, and various proprietary topicals containing mercury are popular over-the-counter remedies. The topical anesthetics benzocaine, dibucaine (Nupercaine), and cyc10methycaine (Surfacaine) are well-known sensitizers. Inasmuch as these are inactive when applied to the skin, and therefore are worthless from the point of dermatologic therapy, it is difficult to understand their popularity. Unfortunately, not only do patients buy them, a significant number of physicians still employ topical anesthetics in treating skin disease. AntihistaInines resemble anesthetics in being inactive when used topically and sometimes producing contact dermatitis. Methapyrilene (Histadil) and tripelennamine (PyribenzaInine) are the problematic ones in my experience. One manufacturer has managed to combine two potent sensitizers in the product called Surfadil which contains Surfacaine and Histadil, thus doubling the chance of sensitivity reactions while marketing a product without therapeutic effect. Dermatitis from acne remedies is not rare in teenagers, and is usually the result of irritation from abrasives, salicylic acid, sulfur, etc., which are common to acne remedies. Occasionally a true allergic contact dermatitis is caused by sensitization to such agents as benzoyl peroxide.
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Fi g. 2
F ig. 3
Fig. 4 Figu r 2 . eo rnyc in con tac t d errnatiti in a 13 . ea r old girl r e m b ling a pyod rma or n u m m u la r ecze ma. D rmatiti b ga n when th e patient a p plie d an ointment con ta in ing neom ycin to a m all a b ra ion of th leu . Th e re ultin g con tac t d ermatiti wa tr eated with a n ot he r n eom ycin topical b y h er p di atrici an , who di a gno ed imp ti go . Th e patch t t with 20 per c nt n omycin \ a tron gl y po iti ve. Appl yin g a orti co teroid a nd toppin g a ll neo m ycin topi cal ' r ult d in rapid clea ring. co myc in con tac t d rmatiti r ultin g from a p plica tio n of a n ointm nt on igur 3. tai n ing neo mycin to a minim al. n on specific int er trigo. tron g po iti ve patch t t to 2 0 p r c nt neo mycin. Figur 4 . eom ci n a llerg o m p licating a topic ecz m a o nb knov nst to th ph y ici an . t h pat i n r' mo t her ha d be en a ppl in g a propriet ary ointm nt co n ta in ing n eom ycin in addi tio n to th e pre cribed topi cal teroid . tr on gl po iti v pa t h te t to 20 p r ce n t n o rnyci n . Wit h e li mina tio n of n eom ycin . th er wa pr ompt cl earin g of th cz rn a with topic al cortico te roid .
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Fi gure 5. Contact dermatiti re ultin z from a lip pom ad e u ed to con trol "c ha pped lip ." Pat ch te tin g \ ith com pone n t of th e pom ad e r veal d th e a lle r e n to be hexa chloroph en a n infrequent en itizer .
This ha been only a brief ummary of topical medicament a a cau e, rather than a cure of dermatitis. Two point require emphasi : 1. Aggravation of a dermatiti with u e of a new topical medicament doe not e tabli h allergy to that medicament ince there are many other rea on wh a dermatiti may flare. Howe r, it hould make a phy ician u piciou of en itization and con ider patch te ting or elimination of the u pected agent ( ig. 5). 2. Topical medicament aller y may be 0 ubtly uperimposed on another dermatiti that the exi tence of a contact dermatitis to a topical medicament is not u pected.
Shoes Shoe contact dermatitis in children i not rare. ore often than not it is mi diagno ed a fungu infection, eczema, or poria i . Proper patch te ting with components of the shoes i neces ary for diagnosi . Shoe contact dermatiti tends to in 01 e the dor a and top of the toe , while sparing the interdigital pace. However, all too often thi almo t dia no tic picture i not present in pro en hoe allergy. The diagno i of hoe contact dermatiti can be ery difficult, a hoe allergy may complicate or co-exist with eczema or poria i of the feet. Since hoe allergy, unlike eczema or poria i ,i a curable condition it i important not to 0 erlook it. Patch t ting for hoe allergy hould be performed with portion of each pair of footwear a well a rubber additi es and chromate I:! ( ig . 6, 7 8 , 9).
ickel ickel allergy i not rare in teenage girl and i often the re ult of sen itization from having their ear pierced. " nick I i a widely u ed metal, a broad range of objects uch a bracelets, necklace ,rings , garter nap , etc., may cause dermatiti. ickel en itization from ear piercing
Fi g. 6
Fi g. 7
Fi gure 6. h oe on tac t derrnatiti in a n 11 yea r old rirl with la s ica l sym me t rica l di .tr ibu tlon over th dor a of th • to a nd th m edi al a pect of th e gr at to . Th co nd ition was tr a t d for . ea rs a recalcit rant a to pic cze rna (t h e patient had both a thma a n d a topic ecze ma in infanc y) a n d had becom e econ da r ily e ns itized to n eom ycin a n d e t hy l n di arnin co n ta in d in topi a l m edicament . tr on rly po iti ve pat ch te t to linin g m at erial of m an of h er hoe ( Fig. 7). uitabl e footwear r ult ed in co m pl te a n d la tin g cI a ring of th d rm atiti s ( ee a ls o color plat e III ). nt hown in F'igur 6. ore tron a rea tion (red \ hil e ot her fail ed to r ac t. Pat ch t tin g h r i not mu t b di ca rd d a nd whi ch mi ght be tol erat d
Fi gu r ru t d. oozin g a nd ec on da rily infect ed ho e co n tac t d rrnatiti which had bee n tr eat ed b . a ph ician a "a t h le te' foot." The c lin i a l a p p a ra nce i quit non pecif a nd i co m pa tib le with a va rie ty of di a gno . Pat ch te t (F ig. ) es ta bli hed th di a gn o i of ho con tac t dermatiti . Fi gur Pat ch te t re ult in th patient hown in Fi gure 8. tron g po sirivc r ac tion to rubb r-and-canva typ port ho e a nd th rubb er a dd itive 'IBT (rn e rca ptobe n zorh ia zole) .
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Figure 10. ickel contact dermatiti having the appearance of a low -grade infection. Strongly po itiv pa tch te t to nickel. ickel allergy apparently resulted from ear piercing and us of metal tu d to keep the tract open. Thi u n fort u na te complication of ear pi rcing can be prevented by u ing a nonmetallic sutu re in t he pierced ear until epithelialization of the tract i com plete (see a l 0 co lor plate III E ).
i to be deplored and can be avoided by using a non-metallic suture instead of a metal stud to keep the inus tract open after piercing ( ig. 10 ). Cosmetics
Cosmetics are not a common cause of contact dermatiti in children, but occasionally one does see a girl who has a rash traceable to eye shadow , face cream , nail polish, or similar cosmetics. Having the patient eliminate all cosmetics and, after clearing of the dermatitis , reintroducing one cosmetic at a time until the dermatitis recurs is the simplest way to clinch the diagnosis. Such a " u sa ge test" er es to convince the patient, as well as the physician, of the causative role of the cosmetic.
MANAGEMENT OF CO TACT DERMATITIS Management of contact dermatitis may be conveniently divided into two often overlapping phases: treating the acute episode and preventin g fu ture episodes of dermatitis. In clearing a contact dermatitis, it is e sential that there be no further contact with the offending agent. Achieving this may be relati ely simple , as with acute poison oak contact dermatitis , or exceedingly complex, for example in shoe contact dermatitis. A rational approach to the problem of insuring that contact with the offending
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agent has ceased requires some knowledge of the nature of the allergen. If the allergen is not identified with reasonable certainty by the clinical
picture, patch testing is indicated. Patch testing is absolutely essential in the management of complex cases of contact dermatitis, whether in children or adults. Thus for example in shoe contact dermatitis, the patch test not only proves the diagnosis, but frequently gives specific information as to the nature of the allergen, whether chrome in the leather, rubber in the lining materials, adhesive, or dyes. In complex cases, patch testing provides the physician with objectively derived facts rather than clinical guesses as a basis for management. Active treatment of contact dermatitis can be summarized in one word: corticosteroids. In severe acute contact dermatitis with vesiculation and edema, topical corticosteroids are without value and systemic steroids may be used. Such severe dermatitis occurs chiefly with plant contact dermatitis; a short course of systemic steroids can produce dramatic relief in 24 to 48 hours and avoid a possible 2 to 3 weeks of miserable dermatitis. I prefer to use prednisone by mouth, usually starting with a dose of 60 mg. per day and decreasing by either 5 mg. or 10 mg. a day so as to complete the course in 7 to 10 days. In very severe cases larger quantities should be used, and I may initiate treatment with 100 mg. of prednisone a day. Giving the entire day's prednisone dose at one time in the morning is effective and convenient. To provide a more rapid onset-and also for its psychological effect-in severe cases I often inject 4 mg. of dexamethasone intramuscularly at the initial office visit. There are many corticosteroids besides prednisone available, but they are all more expensive and possess no advantages. The ready prepared "dosage packs" of corticosteroids are best avoided since the daily corticosteroid dosage provided is too low. Some prefer to use ACTH injections when a systemic corticosteroid is required. While effective, ACTH therapy has the drawbacks of requiring injections and repeated office visits. Physicians concerned about giving high doses of corticosteroids should recall that the side-effects of corticosteroids are related mainly to the length of treatment rather than to treatment intensity. A short 7 to 10 day course of high dosage, rapidly tapered prednisone is well tolerated. Peptic ulceration is the only significant contraindication. I have employed such brief 7 to 10 day courses of systemic prednisone in literally thousands of patients with acute plant contact dermatitis without difficulty. The important principle is to use sufficient corticosteroid to gain control of the inflammatory process, then promptly and steadily decrease the daily dose. In children, acute plant contact dermatitis is practically the only type of contact dermatitis requiring systemic corticosteroids. In other types of contact dermatitis, topical corticosteroids alone usually suffice. In the initial stages of an acute contact dermatitis, when topical corticosteroids are without value, cool compresses with tap water, Burow's solution, dilute white vinegar, or similar nonstaining liquid will soothe and help remove crusts. I prefer a mixture of 1f4 cup (60 ml.) of white vinegar with 2 quarts of cold water. I am not sure that this is
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superior to plain water, but the patients feel they are using a "medicine." Any bouts of localized itching are best controlled by the application of cold in the form of ice cubes or a plastic bag containing ice water. I don't like the Calamine type of shake lotion and similar proprietary over-the-counter poison oak remedies; their chief effect is to leave a messy residue on the skin. Topical antihistamines and topical anesthetics are to be avoided since they are without benefit and may sensitize. For those patients with milder contact dermatitis, and in the subacute and chronic stages of a severe dermatitis, topical corticosteroids are effective. I no longer use hydrocortisone; the newer corticosteroids':' are far superior to and often less expensive than comparable hydrocortisone preparations. The majority of patients will prefer a cream - by this is meant any water-washable non-greasy base - applied very thinly with the fingers 4 to 10 times daily and massaged in well. Patients often apply a topical steroid only 2 or 3 times a day, feeling that this suffices. Sometimes it does, but better results are obtained with more frequent applications. In the chronic stages of a contact dermatitis, particularly when there is dryness, marked thickening and fissuring, a steroid ointment is preferable. Unlike the creams, ointments are greasy bases which leave a film on the skin. This film is usually not objectionable, provided that the ointments are applied very sparingly. In my experience, chronic shoe contact dermatitis is practically the only time a greasy steroid ointment is indicated in the treatment of contact dermatitis in children. Secondary infection with crusting, oozing, swelling, and pain may complicate contact dermatitis, especially on the feet. As blisters, crusts, swelling and similar hallmarks of infection can also occur in acute contact dermatitis, it is sometimes impossible to determine whether or not secondary infection is present. When infection is present or suspected, a systemic antibiotic is indicated. My preference in this situation is erythromycin, or a semisynthetic penicillin such as dicloxacillin, by mouth. I try to avoid ordinary penicillin with its injections and risk of sensitization. Systemic antihistamines and other internal "anti-itch" remedies are touted in advertisements as being effective in contact dermatitis. None of these preparations affects itching; nor do they suppress inflammation. They act solely by virtue of their sedative effect. When the allergic response is properly suppressed by the use of corticosteroids, they are unnecessary.
PREVENTION Prevention of future episodes of contact dermatitis depends on avoiding future contact with the offending agent since desensitization 'Double-blind studies have shown that triamcinolone (Aristocort, Kenalog), flurandrenolone (Cordran), fluocinolone (Synalar) and betamethasone valirate (Valisone) are all much more effective than hydrocortisone. This is not true of dexamethasone (Decadron) although this has been advertised as a superior fluorinated steroid. Topical corticosteroids are expensive; the physician will be doing his patients a favor to occasionally compare prices. My personal feeling is that the current "best buys" are Cordran 0.025%, Aristocort 0.025% and Kenalog 0.025%.
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procedures are not effective. Avoiding further contact with an identified allergen may be simple, when the allergen is a topical medicament such as neomycin, or on the other hand very difficult. Preventing a recurrence of shoe contact dermatitis is an example of a very difficult situation. Rubber additives are the most frequently identified cause of shoe allergy, and these agents are found in the adhesives or lining materials of virtually all footwear. The importance of identifying the allergen deserves repeat emphasis since one can only avoid offenders if they are known. Adjunctive measures may sometimes effectively prevent or minimize recurrences of contact dermatitis. Frequent use of a topical corticosteroid will often enable a patient to tolerate shoes, or a garment, to which they are allergic and which would otherwise produce significant dermatitis. Use of an absorbent foot powder will help prevent shoe dermatitis by minimizing the sweat leaching out allergens from the shoe. These and similar measures are fully discussed by Fischer. 7 Much has been written on the vexing problem of preventing recurrences of Rhus contact dermatitis in areas where poison ivy or poison oak abounds. Instructions as to the appearance of the plant and the wearing of protective clothing are helpful. The traditional scrub with strong laundry soap is to be condemned, since a mild soap will cleanse equally well and avoid skin irritation. The benefits of washing in preventing poison oak dermatitis have been overrated. It has been demonstrated that washing must be accomplished within 30 minutes of exposure to have any beneficial effect. After that time the allergen becomes firmly affixed and cannot be dislodged by washing. Desensitization is not the answer for poison oak dermatitis, or any other contact dermatitis. There are numerous commercial preparations claiming to "desensitize" those allergic to plants of the Rhus family. Most are completely inactive and consequently ineffective. There are a few potent preparations available, which, when given in adequate dosage, will produce a demonstrable but temporary decrease in the degree of hypersensitivity. The drawback to these preparations is that adequate dosages usually produce side-effects such as rectal itching or generalized eruptions and itching. Furthermore, there have been reports of serious kidney damage from potent injected Rhus extracts. I neither use nor recommend Rhus desensitization. It is simpler and more effective to treat each of multiple episodes of poison oak contact dermatitis with short courses of systemic corticosteroids.
SUMMARY Except for acute plant contact dermatitis from members of the Rhus family, allergic contact dermatitis in children is infrequent. Most cases of contact dermatitis in children can be managed by the clinician without resorting to patch testing. Clinicians tend to overdiagnose allergic contact dermatitis in children.
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In children, the most commonly encountered causes of contact dermatitis in the United States appear to be: (1) plants of the Rhus famil::, (2) topical medicaments, (3) shoes, (4) nickel, and (5) cosmetics. In complex situations, especially in susperted shoe contact dermatitIS, properly performed patch testing is essenr.'al for accurate diagnosis and effective therapy. Corticosteroids are the essential drugs in t:tp treatment of contact dePllatitis. In the severe acute cases short cou.·se,~ of systemic steroids are dramatically effective. In sub-acute or chrcnic dermatoses, topical corti-::osteroids alone will usuaLy suffice. Avoidance of further contact with the allergen is the only effective way of preventing contact dermatitis since desensitization is not practical or effective.
REFERENCES 1. Calnan. C. D.: The climate of contact dermatitis. Acta Dermatovener., 44:33-43, 1964. 2. Cronin, E., Bandmann, J. H., Calnan, C. D., et al.: Contact dermatitis in the atopic. Acta Dermatovener., 50:183-187,1970. 3. Epstein, E.: Allergy to dermatologic agents. J.A.M.A., 198:517-520,1966. 4. Epstein, E.: Detection of neomycin sensitivity. Arch. Derm., 91 :50-53, 1965. 5. Epstein, E.: Shoe contact dermatitis. J.A.M.A., 209:1487-1492,1969. 6. Epstein, E.: Simplified photopatch testing. Arch. Derm., 93:217-220,1966. 7. Fisher, A. A.: Contact Dermatitis. Philadelphia, Lea and Febiger, 1967. 8. Gaul, L. E.: Development of allergic nickel dermatitis from earrings. J.A.M.A., 200:186188, 1967. 9. Harber, L. C., Harris, H., and Baer, R. L.: Photoallergic contact dermatitis. Arch. Derm., 94:255-262, 1966. 10. Hjorth, N., and Gregert, S.: Contact dermatitis. In Rook, R., Wilkinson, D. S., and Ebling, F. J. G., eds.: Textbook of Dermatology. Philadelphia, F. A. Davis, 1968. 11. Lowney, E. D.: Dermatologic implications of immunological unresponsiveness. J. Invest. Derm., 54:355-364, 1970. 12. Magnusson, B., and Hersle, K.: Patch test methods. 1. A comparative study of six different types of patch tests. Acta Dermatovener., 45: 123-128, 1965. 13. Magnusson, B., and Hersle, K.: Patch test methods. II. Regional variations of patch test responses. Acta Dermatovener., 45:257-261,1965. San Mateo Medical Clinic 23 Baldwin Avenue San Mateo, California 94401
Contact Dermatitis in Children
Ernst Epstein, M.D. *
A chemical can cause contact dermatitis by two fundamentally different mechanisms - irritancy and allergy. 7 , 10 Irritant dermatitis, usually called primary irritant dermatitis, results from nonspecific skin injury. Acids, strong alkalies, and detergents are examples of irritants capable of causing primary irritant dermatitis by a nonspecific skininjuring effect. The allergic type of contact dermatitis depends on the existence of a specific antibody. The patient will not react with allergic contact dermatitis unless allergy, an acquired specific alteration in the capacity to react, exists. Poison ivy and poison oak are common causes of allergic contact dermatitis in North America. Generally when dermatologists refer to contact dermatitis they mean allergic contact dermatitis. Allergic contact dermatitis is clinically the more significant type of contact dermatitis, and this discussion will be limited to it. For brevity we will use the phrase "contact dermatitis" to mean "allergic contact dermatitis."
FUNDAMENT AL ASPECTS Allergic contact dermatitis is a true allergic process resulting from an antibody-antigen reaction. The antibody responsible for allergic contact dermatitis is fixed to cells of the lymphoid system. This type of fixed antibody produces a reaction only after a delay of hours or days after contact with the antigen. Hence this type of allergy is referred to as delayed, or "contact type," allergy. Because the antibodies are fixed to cells, serologic tests are of no value, and it is necessary to apply the allergen to living tissue to detect the presence of antibody. Delayed allergy is responsible for the tuberculin test in which the antigen (tuberculin) is either injected into the skin (Mantoux test) or applied to the skin (Vollmer's test) as a patch test. After a delay of 48 to 72 hours, a reaction is apparent if allergy exists. While both the intradermal and patch tests are theoretically suitable for detecting contact type allergy, "'Clinical Assistant Professor of Dermatology, University of California, San Francisco Medical Center
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in the investigation of contact dermatitis only the patch test method is practicaL" Delayed or contact type allergy is, like other allergies,· acquired. Sensitization is a complex process, depending both on exposure and the innate ability to become sensitized. Much work has been done on experimental sensitization, and ways of preventing it. In animals, and apparently in man, it is possible to prevent or minimize sensitization by suitable pretreatment with the allergen. l l There has been much debate whether patients with certain dermatologic disorders, particularly atopic eczema, are more prone to develop contact sensitization than normal individuals. It has been clearly demonstrated that inflamed or dermatitic skin is more prone to sensitization than intact skin. However, it appears that patients with atopic dermatitis are no more prone to develop contact allergy than patients with eczematous dermatoses of other etiology.2 Delayed or contact type allergy is fundamentally different from immediate or anaphylactic sensitiv:ity. In immediate allergy we are dealing with a circulating antibody which produces a whealing reaction within minutes after scratch or intradermal testing. Urticaria and anaphylaxis are reactions caused when immediate type antibody reacts with antigen. The immediate type of allergy has nothing to do with contact dermatitis, and scratch and intradermal testing for immediate type allergy are of no value in the diagnosis of contact dermatitis. Atopic dermatitis and contact dermatitis are sometimes confused. These are two distinct and unrelated entities, which may co-exist. Atopic dermatitis (also called constitutional eczema) is an inborn defect, the nature of which is unknown. Atopic dermatitis is not an allergic disease, although it is often, and incorrectly, referred to as "allergic eczema" or "skin allergy." The patient with atopic eczema characteristically has dry skin, abnormalities in reactivity of the skin vasculature, sensitivity to irritants such as rough clothing, as well as circulating antibodies of the immediate whealing type to a variable number of substances. The relationship of the atopic antibodies, or reagins, to the patient's eczema is in most cases uncertain. It is clear that nonspecific measures such as topical steroids, skin lubrication, and avoiding irritants are far more successful in controlling atopic dermatitis than desensitization or elimination techniques directed toward atopic allergens discovered by scratch and intradermal testing. Another area of confusion is the meaning of the word eczema. Eczema is a morphologic term describing a reaction pattern, and is not a diagnosis. Dermatologists use the word eczema to describe a nonspecific inflammatory reaction of the skin manifesting erythema, scaling and varying degrees of exudative change. Unfortunately some physicians consider the term eczema as synonymous with atopic dermatitis. Using the word eczema to mean atopic dermatitis is both incorrect and con*Intradermal testing for contact allergy can be performed with certain allergens which are water soluble and non-irritating under test conditions. However" in contact dermatitis, the intradermal test is generally a research tool.
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fusing, since eczema may result from many processes besides the atopic state. Eczema remains a very useful term to describe a cutaneous reaction pattern. Eczema and dermatitis have essentially the same meaning, British authors usually preferring dermatitis.
DIAGNOSIS The diagnosis of allergic contact dermatitis is based essentially on the history and physical findings, particularly the distribution of the eruption. The patch test is the only test available for the investigation of contact dermatitis. The patch test is tricky, both in execution and interpretation, and is best left to experts. Fortunately, when contact dermatitis occurs in children, patch testing is usually not necessary. Often the diagnosis of allergic contact dermatitis is evident at once-for example, a patchy, streaky vesicular contact dermatitis in a youngster who has been in the woods of California is almost certainly caused by poison oak. On the other hand, the diagnosis may be exceedingly difficult, as when allergy to a topically applied medicament complicates a pre-existing dermatitis such as atopic eczema. In complicated situations, a high degree of clinical suspicion combined with shrewd observations and careful patch testing is necessary to sort out the complex events occurring in the skin. There are two aspects to making a diagnosis of contact dermatitis: (1) Is the dermatitis a contact dermatitis, and (2) if so, what is the contactant responsible? In the differential diagnosis of contact dermatitis, the distribution and patterning of the lesions is often of more help than the morphology of the lesion itself. Contact dermatitis is often an eczematous process, the individual patches of which may be quite indistinguishable from eczematous dermatitis of endogenous cause such as atopic or seborrheic dermatitis. When extensive, it may be difficult to distinguish contact dermatitis from a drug eruption. Furthermore, there is no consistent way of judging, from the appearance, whether a dermatitis is an allergic contact dermatitis or the result of nonspecific skin irritation. The distribution and patterning of allergic contact dermatitis frequently provides useful clues. For example, plants of the Rhus (poison ivy, poison oak) usually produce a streaky, patchy, very acute dermatitis on exposed areas. The history may be very important in the diagnosis of contact dermatitis; it usually must be a directed history, following up leads suggested by the clinical appearance of the eruption. If a plant contact dermatitis is suspected, questioning as to contact with brush, pets who have roamed in the woods, etc., is indicated. On the other hand, if one suspects a topical medicament, intensive inquiry as to self-treatment and previous medical therapy with topicals is necessary. Sometimes considerable skill and a great deal of persistence are needed to ferret out the answer. It should be emphasized that in this situation, examination and history complement and supplement each other, and repeated attempts are often necessary to elicit the significant information.
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Most physicians treating children tend to overdiagnose contact dermatitis. All too often a patch of atopic eczema. a persisting diaper dermatitis, or skin that has become irritated from excessive soap and water scrubbing is labeled as contact dermatitis. Except for acute plant contact dermatitis to the Rhus family, allergic contact dermatitis is not common in children. Most eczematous dermatoses of children are the result of endogenous factors (atopic or seborrheic) combined with nonspecific irritant effects of soap, water, rough clothing, etc.
PATCH TESTING Patch testing is of great value when investigating an obscure case of suspected contact dermatitis. 7 ,lO In principle, the test is simple; the suspected agent is applied to the skin under an occlusive dressing for 48 hours. Inflammation at the test site indicates allergy. While the principle of the patch test is simple, in practice it is quite complex. 1 Not only does the result of patch testing differ with the skin site and test covering used,12,13 to further complicate matters, false-negative and false-positive test results may occur. Many commonly used substances which do not irritate in ordinary usage, such as tincture of Zephiran, or shampoos, may cause nonspecific false-positive irritant reactions under the conditions of the patch test. On the other hand, certain substances such as neomycin will give false-negative patch tests in patients allergic to them. When the usual commercial ointment containing 0.5 per cent neomycin is used in the patch test, at least 50 per cent of patients with proven neomycin allergy will have a negative test. 4 One of the reasons for false-negative results is that patch testing must be done on intact skin, which is less reactive than the inflamed skin to which the topical medicament is applied. In the case of neomycin, the correct patch test concentration is 20 per cent! The complexities and pitfalls of patch testing are well discussed by Fisher 7 and by Hjorth and Fregert. 10 Patch testing is best left to those with experience with this tricky biological test.
PHOTO CONTACT DERMATITIS A fascinating variant of allergic contact dermatitis is photo contact dermatitis. In this situation, an agent sensitizes the skin surface to sunlight. Dermatitis from contact with the photosensitizing allergen occurs only in the presence of sufficient light. The compounds causing a photo contact dermatitis are essentially limited to certain topical antiseptics such as the brominated salicylanilides added to some of the antiseptic soaps. In my experience, photo contact dermatitis in children is rare. In photo contact dermatitis ordinary patch tests may be negative. It is usually necessary to have the patch test site exposed to suitable light after removal of the patch test, and to read the test result 24 hours after the light exposure. 6 , 9
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CAUSES OF CO TACT DERMATITIS In children the mo t common cau es of contact dermatiti encountered in orthern California are plant (poi on oak), topical medicamen t , hoe , n ic kel, and cosmetic . Plants In orthern California, the va t majority of ca e of contact dermatitis in children are caused by the plant of the Rhu family known as poi on oak (Fig. 1). Any patient allergic to one member of the Rhu family (poi on oak, poison ivy, poison sumac) i allergic to the other . Furthermore , the aller ic component of mangoe and the Japane e lacqu er tree cro -reac t with the Rhu allergen. In many patient with acute poi on oak con ta c t dermatiti the diagnosi i ea y and in fact ha u ually been m ad e b the patient. Exposure to bru h , followed by treak and patche of a cu te dermatiti , i practically diagno tic. Howe er, wh n contact with the plant i indirect uch a from a pet that h a roamed the wood , the dermatiti tend to be more diffuse and the diagno i may be difficult unle uch indirect ource of expo ure are u pected. U ually poi on oak con ta ct dermatiti appear 1 to 3 day after expo ure. Howe er, in tho e patient pre iou ly not allergic to poi on oak who become ensiti zed a a re ult of their exposure, the eruption appear only after a latent period of 9 to 14 day or more. The pattern of dermatiti in the e patient where the exposure is both en iti.zin.q and elic it in g tend to be different than in tho e patient with e tabli hed allergy. In tead of rapid de elopment of the dermatiti there tend to be a low increa e in e erity of the dermatiti a the patient' fixed antibodie increa e. Because of the more prolonged cour e of the dermatitis , longer period of y temic corticoteroid therapy are often required to control the dermatiti .
Figure 1. c u te pla n t co n tac t dermat iti from poi on oak wit h c harac teri tic tr ea k and patc he of ve icula r de rm at iti ( ee a l 0 color plate IIIB ).
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In areas where ragweed abounds, ragweed may cause a stubborn, chronic, but definitely seasonal contact dermatitis frequently incorrectly diagnosed as endogenous eczema (neurodermatitis). This is uncommon in children. The offending agent is a fat soluble oily fraction of the ragweed plant quite distinct from the allergen causing hay fever and asthma which are caused by a water soluble protein fraction of the ragweed plant.
Topical Medicaments These are probably the next most common cause of contact dermatitis in children. It is difficult to make firm statements as to which topical medicaments are the most common offenders since this depends both on the pattern of usage, and the sensitizing capacity of the medicament. 3 For example, penicillin applied topically is a very potent sensitizer; yet we do not see contact dermatitis from penicillin since penicillin ointments were withdrawn from usage years ago. Currently in Northern California, neomycin, ethylenediamine, and thimerosal (Merthiolate) are the most common troublemakers. Neomycin allergy is frequently hard to diagnose since it often produces only a chronic aggravation of the underlying skin disorder and is suspected by neither patient nor physician (Figs. 2, 3, 4). EthylenediaInine is an excipient found in only one medicament, Mycolog cream. Mycolog cream also contains neomycin, a second potent sensitizer. Thimerosal (Merthiolate) produces its share of dermatitis because patients are fond of painting it on their rashes. Although thimerosal contains mercury, patients allergic to thimerosal are sensitive to the organic part of the molecule and not to mercury. On the other hand, patients allergic to merbroInin (Mercurochrome) are allergic to mercury. Mercury allergy is still an occasional problem, as ammoniated mercury, yellow oxide of mercury, and various proprietary topicals containing mercury are popular over-the-counter remedies. The topical anesthetics benzocaine, dibucaine (Nupercaine), and cyc10methycaine (Surfacaine) are well-known sensitizers. Inasmuch as these are inactive when applied to the skin, and therefore are worthless from the point of dermatologic therapy, it is difficult to understand their popularity. Unfortunately, not only do patients buy them, a significant number of physicians still employ topical anesthetics in treating skin disease. AntihistaInines resemble anesthetics in being inactive when used topically and sometimes producing contact dermatitis. Methapyrilene (Histadil) and tripelennamine (PyribenzaInine) are the problematic ones in my experience. One manufacturer has managed to combine two potent sensitizers in the product called Surfadil which contains Surfacaine and Histadil, thus doubling the chance of sensitivity reactions while marketing a product without therapeutic effect. Dermatitis from acne remedies is not rare in teenagers, and is usually the result of irritation from abrasives, salicylic acid, sulfur, etc., which are common to acne remedies. Occasionally a true allergic contact dermatitis is caused by sensitization to such agents as benzoyl peroxide.
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Fi g. 2
F ig. 3
Fig. 4 Figu r 2 . eo rnyc in con tac t d errnatiti in a 13 . ea r old girl r e m b ling a pyod rma or n u m m u la r ecze ma. D rmatiti b ga n when th e patient a p plie d an ointment con ta in ing neom ycin to a m all a b ra ion of th leu . Th e re ultin g con tac t d ermatiti wa tr eated with a n ot he r n eom ycin topical b y h er p di atrici an , who di a gno ed imp ti go . Th e patch t t with 20 per c nt n omycin \ a tron gl y po iti ve. Appl yin g a orti co teroid a nd toppin g a ll neo m ycin topi cal ' r ult d in rapid clea ring. co myc in con tac t d rmatiti r ultin g from a p plica tio n of a n ointm nt on igur 3. tai n ing neo mycin to a minim al. n on specific int er trigo. tron g po iti ve patch t t to 2 0 p r c nt neo mycin. Figur 4 . eom ci n a llerg o m p licating a topic ecz m a o nb knov nst to th ph y ici an . t h pat i n r' mo t her ha d be en a ppl in g a propriet ary ointm nt co n ta in ing n eom ycin in addi tio n to th e pre cribed topi cal teroid . tr on gl po iti v pa t h te t to 20 p r ce n t n o rnyci n . Wit h e li mina tio n of n eom ycin . th er wa pr ompt cl earin g of th cz rn a with topic al cortico te roid .
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Fi gure 5. Contact dermatiti re ultin z from a lip pom ad e u ed to con trol "c ha pped lip ." Pat ch te tin g \ ith com pone n t of th e pom ad e r veal d th e a lle r e n to be hexa chloroph en a n infrequent en itizer .
This ha been only a brief ummary of topical medicament a a cau e, rather than a cure of dermatitis. Two point require emphasi : 1. Aggravation of a dermatiti with u e of a new topical medicament doe not e tabli h allergy to that medicament ince there are many other rea on wh a dermatiti may flare. Howe r, it hould make a phy ician u piciou of en itization and con ider patch te ting or elimination of the u pected agent ( ig. 5). 2. Topical medicament aller y may be 0 ubtly uperimposed on another dermatiti that the exi tence of a contact dermatitis to a topical medicament is not u pected.
Shoes Shoe contact dermatitis in children i not rare. ore often than not it is mi diagno ed a fungu infection, eczema, or poria i . Proper patch te ting with components of the shoes i neces ary for diagnosi . Shoe contact dermatiti tends to in 01 e the dor a and top of the toe , while sparing the interdigital pace. However, all too often thi almo t dia no tic picture i not present in pro en hoe allergy. The diagno i of hoe contact dermatiti can be ery difficult, a hoe allergy may complicate or co-exist with eczema or poria i of the feet. Since hoe allergy, unlike eczema or poria i ,i a curable condition it i important not to 0 erlook it. Patch t ting for hoe allergy hould be performed with portion of each pair of footwear a well a rubber additi es and chromate I:! ( ig . 6, 7 8 , 9).
ickel ickel allergy i not rare in teenage girl and i often the re ult of sen itization from having their ear pierced. " nick I i a widely u ed metal, a broad range of objects uch a bracelets, necklace ,rings , garter nap , etc., may cause dermatiti. ickel en itization from ear piercing
Fi g. 6
Fi g. 7
Fi gure 6. h oe on tac t derrnatiti in a n 11 yea r old rirl with la s ica l sym me t rica l di .tr ibu tlon over th dor a of th • to a nd th m edi al a pect of th e gr at to . Th co nd ition was tr a t d for . ea rs a recalcit rant a to pic cze rna (t h e patient had both a thma a n d a topic ecze ma in infanc y) a n d had becom e econ da r ily e ns itized to n eom ycin a n d e t hy l n di arnin co n ta in d in topi a l m edicament . tr on rly po iti ve pat ch te t to linin g m at erial of m an of h er hoe ( Fig. 7). uitabl e footwear r ult ed in co m pl te a n d la tin g cI a ring of th d rm atiti s ( ee a ls o color plat e III ). nt hown in F'igur 6. ore tron a rea tion (red \ hil e ot her fail ed to r ac t. Pat ch t tin g h r i not mu t b di ca rd d a nd whi ch mi ght be tol erat d
Fi gu r ru t d. oozin g a nd ec on da rily infect ed ho e co n tac t d rrnatiti which had bee n tr eat ed b . a ph ician a "a t h le te' foot." The c lin i a l a p p a ra nce i quit non pecif a nd i co m pa tib le with a va rie ty of di a gno . Pat ch te t (F ig. ) es ta bli hed th di a gn o i of ho con tac t dermatiti . Fi gur Pat ch te t re ult in th patient hown in Fi gure 8. tron g po sirivc r ac tion to rubb r-and-canva typ port ho e a nd th rubb er a dd itive 'IBT (rn e rca ptobe n zorh ia zole) .
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Figure 10. ickel contact dermatiti having the appearance of a low -grade infection. Strongly po itiv pa tch te t to nickel. ickel allergy apparently resulted from ear piercing and us of metal tu d to keep the tract open. Thi u n fort u na te complication of ear pi rcing can be prevented by u ing a nonmetallic sutu re in t he pierced ear until epithelialization of the tract i com plete (see a l 0 co lor plate III E ).
i to be deplored and can be avoided by using a non-metallic suture instead of a metal stud to keep the inus tract open after piercing ( ig. 10 ). Cosmetics
Cosmetics are not a common cause of contact dermatiti in children, but occasionally one does see a girl who has a rash traceable to eye shadow , face cream , nail polish, or similar cosmetics. Having the patient eliminate all cosmetics and, after clearing of the dermatitis , reintroducing one cosmetic at a time until the dermatitis recurs is the simplest way to clinch the diagnosis. Such a " u sa ge test" er es to convince the patient, as well as the physician, of the causative role of the cosmetic.
MANAGEMENT OF CO TACT DERMATITIS Management of contact dermatitis may be conveniently divided into two often overlapping phases: treating the acute episode and preventin g fu ture episodes of dermatitis. In clearing a contact dermatitis, it is e sential that there be no further contact with the offending agent. Achieving this may be relati ely simple , as with acute poison oak contact dermatitis , or exceedingly complex, for example in shoe contact dermatitis. A rational approach to the problem of insuring that contact with the offending
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agent has ceased requires some knowledge of the nature of the allergen. If the allergen is not identified with reasonable certainty by the clinical
picture, patch testing is indicated. Patch testing is absolutely essential in the management of complex cases of contact dermatitis, whether in children or adults. Thus for example in shoe contact dermatitis, the patch test not only proves the diagnosis, but frequently gives specific information as to the nature of the allergen, whether chrome in the leather, rubber in the lining materials, adhesive, or dyes. In complex cases, patch testing provides the physician with objectively derived facts rather than clinical guesses as a basis for management. Active treatment of contact dermatitis can be summarized in one word: corticosteroids. In severe acute contact dermatitis with vesiculation and edema, topical corticosteroids are without value and systemic steroids may be used. Such severe dermatitis occurs chiefly with plant contact dermatitis; a short course of systemic steroids can produce dramatic relief in 24 to 48 hours and avoid a possible 2 to 3 weeks of miserable dermatitis. I prefer to use prednisone by mouth, usually starting with a dose of 60 mg. per day and decreasing by either 5 mg. or 10 mg. a day so as to complete the course in 7 to 10 days. In very severe cases larger quantities should be used, and I may initiate treatment with 100 mg. of prednisone a day. Giving the entire day's prednisone dose at one time in the morning is effective and convenient. To provide a more rapid onset-and also for its psychological effect-in severe cases I often inject 4 mg. of dexamethasone intramuscularly at the initial office visit. There are many corticosteroids besides prednisone available, but they are all more expensive and possess no advantages. The ready prepared "dosage packs" of corticosteroids are best avoided since the daily corticosteroid dosage provided is too low. Some prefer to use ACTH injections when a systemic corticosteroid is required. While effective, ACTH therapy has the drawbacks of requiring injections and repeated office visits. Physicians concerned about giving high doses of corticosteroids should recall that the side-effects of corticosteroids are related mainly to the length of treatment rather than to treatment intensity. A short 7 to 10 day course of high dosage, rapidly tapered prednisone is well tolerated. Peptic ulceration is the only significant contraindication. I have employed such brief 7 to 10 day courses of systemic prednisone in literally thousands of patients with acute plant contact dermatitis without difficulty. The important principle is to use sufficient corticosteroid to gain control of the inflammatory process, then promptly and steadily decrease the daily dose. In children, acute plant contact dermatitis is practically the only type of contact dermatitis requiring systemic corticosteroids. In other types of contact dermatitis, topical corticosteroids alone usually suffice. In the initial stages of an acute contact dermatitis, when topical corticosteroids are without value, cool compresses with tap water, Burow's solution, dilute white vinegar, or similar nonstaining liquid will soothe and help remove crusts. I prefer a mixture of 1f4 cup (60 ml.) of white vinegar with 2 quarts of cold water. I am not sure that this is
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superior to plain water, but the patients feel they are using a "medicine." Any bouts of localized itching are best controlled by the application of cold in the form of ice cubes or a plastic bag containing ice water. I don't like the Calamine type of shake lotion and similar proprietary over-the-counter poison oak remedies; their chief effect is to leave a messy residue on the skin. Topical antihistamines and topical anesthetics are to be avoided since they are without benefit and may sensitize. For those patients with milder contact dermatitis, and in the subacute and chronic stages of a severe dermatitis, topical corticosteroids are effective. I no longer use hydrocortisone; the newer corticosteroids':' are far superior to and often less expensive than comparable hydrocortisone preparations. The majority of patients will prefer a cream - by this is meant any water-washable non-greasy base - applied very thinly with the fingers 4 to 10 times daily and massaged in well. Patients often apply a topical steroid only 2 or 3 times a day, feeling that this suffices. Sometimes it does, but better results are obtained with more frequent applications. In the chronic stages of a contact dermatitis, particularly when there is dryness, marked thickening and fissuring, a steroid ointment is preferable. Unlike the creams, ointments are greasy bases which leave a film on the skin. This film is usually not objectionable, provided that the ointments are applied very sparingly. In my experience, chronic shoe contact dermatitis is practically the only time a greasy steroid ointment is indicated in the treatment of contact dermatitis in children. Secondary infection with crusting, oozing, swelling, and pain may complicate contact dermatitis, especially on the feet. As blisters, crusts, swelling and similar hallmarks of infection can also occur in acute contact dermatitis, it is sometimes impossible to determine whether or not secondary infection is present. When infection is present or suspected, a systemic antibiotic is indicated. My preference in this situation is erythromycin, or a semisynthetic penicillin such as dicloxacillin, by mouth. I try to avoid ordinary penicillin with its injections and risk of sensitization. Systemic antihistamines and other internal "anti-itch" remedies are touted in advertisements as being effective in contact dermatitis. None of these preparations affects itching; nor do they suppress inflammation. They act solely by virtue of their sedative effect. When the allergic response is properly suppressed by the use of corticosteroids, they are unnecessary.
PREVENTION Prevention of future episodes of contact dermatitis depends on avoiding future contact with the offending agent since desensitization 'Double-blind studies have shown that triamcinolone (Aristocort, Kenalog), flurandrenolone (Cordran), fluocinolone (Synalar) and betamethasone valirate (Valisone) are all much more effective than hydrocortisone. This is not true of dexamethasone (Decadron) although this has been advertised as a superior fluorinated steroid. Topical corticosteroids are expensive; the physician will be doing his patients a favor to occasionally compare prices. My personal feeling is that the current "best buys" are Cordran 0.025%, Aristocort 0.025% and Kenalog 0.025%.
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procedures are not effective. Avoiding further contact with an identified allergen may be simple, when the allergen is a topical medicament such as neomycin, or on the other hand very difficult. Preventing a recurrence of shoe contact dermatitis is an example of a very difficult situation. Rubber additives are the most frequently identified cause of shoe allergy, and these agents are found in the adhesives or lining materials of virtually all footwear. The importance of identifying the allergen deserves repeat emphasis since one can only avoid offenders if they are known. Adjunctive measures may sometimes effectively prevent or minimize recurrences of contact dermatitis. Frequent use of a topical corticosteroid will often enable a patient to tolerate shoes, or a garment, to which they are allergic and which would otherwise produce significant dermatitis. Use of an absorbent foot powder will help prevent shoe dermatitis by minimizing the sweat leaching out allergens from the shoe. These and similar measures are fully discussed by Fischer. 7 Much has been written on the vexing problem of preventing recurrences of Rhus contact dermatitis in areas where poison ivy or poison oak abounds. Instructions as to the appearance of the plant and the wearing of protective clothing are helpful. The traditional scrub with strong laundry soap is to be condemned, since a mild soap will cleanse equally well and avoid skin irritation. The benefits of washing in preventing poison oak dermatitis have been overrated. It has been demonstrated that washing must be accomplished within 30 minutes of exposure to have any beneficial effect. After that time the allergen becomes firmly affixed and cannot be dislodged by washing. Desensitization is not the answer for poison oak dermatitis, or any other contact dermatitis. There are numerous commercial preparations claiming to "desensitize" those allergic to plants of the Rhus family. Most are completely inactive and consequently ineffective. There are a few potent preparations available, which, when given in adequate dosage, will produce a demonstrable but temporary decrease in the degree of hypersensitivity. The drawback to these preparations is that adequate dosages usually produce side-effects such as rectal itching or generalized eruptions and itching. Furthermore, there have been reports of serious kidney damage from potent injected Rhus extracts. I neither use nor recommend Rhus desensitization. It is simpler and more effective to treat each of multiple episodes of poison oak contact dermatitis with short courses of systemic corticosteroids.
SUMMARY Except for acute plant contact dermatitis from members of the Rhus family, allergic contact dermatitis in children is infrequent. Most cases of contact dermatitis in children can be managed by the clinician without resorting to patch testing. Clinicians tend to overdiagnose allergic contact dermatitis in children.
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In children, the most commonly encountered causes of contact dermatitis in the United States appear to be: (1) plants of the Rhus famil::, (2) topical medicaments, (3) shoes, (4) nickel, and (5) cosmetics. In complex situations, especially in susperted shoe contact dermatitIS, properly performed patch testing is essenr.'al for accurate diagnosis and effective therapy. Corticosteroids are the essential drugs in t:tp treatment of contact dePllatitis. In the severe acute cases short cou.·se,~ of systemic steroids are dramatically effective. In sub-acute or chrcnic dermatoses, topical corti-::osteroids alone will usuaLy suffice. Avoidance of further contact with the allergen is the only effective way of preventing contact dermatitis since desensitization is not practical or effective.
REFERENCES 1. Calnan. C. D.: The climate of contact dermatitis. Acta Dermatovener., 44:33-43, 1964. 2. Cronin, E., Bandmann, J. H., Calnan, C. D., et al.: Contact dermatitis in the atopic. Acta Dermatovener., 50:183-187,1970. 3. Epstein, E.: Allergy to dermatologic agents. J.A.M.A., 198:517-520,1966. 4. Epstein, E.: Detection of neomycin sensitivity. Arch. Derm., 91 :50-53, 1965. 5. Epstein, E.: Shoe contact dermatitis. J.A.M.A., 209:1487-1492,1969. 6. Epstein, E.: Simplified photopatch testing. Arch. Derm., 93:217-220,1966. 7. Fisher, A. A.: Contact Dermatitis. Philadelphia, Lea and Febiger, 1967. 8. Gaul, L. E.: Development of allergic nickel dermatitis from earrings. J.A.M.A., 200:186188, 1967. 9. Harber, L. C., Harris, H., and Baer, R. L.: Photoallergic contact dermatitis. Arch. Derm., 94:255-262, 1966. 10. Hjorth, N., and Gregert, S.: Contact dermatitis. In Rook, R., Wilkinson, D. S., and Ebling, F. J. G., eds.: Textbook of Dermatology. Philadelphia, F. A. Davis, 1968. 11. Lowney, E. D.: Dermatologic implications of immunological unresponsiveness. J. Invest. Derm., 54:355-364, 1970. 12. Magnusson, B., and Hersle, K.: Patch test methods. 1. A comparative study of six different types of patch tests. Acta Dermatovener., 45: 123-128, 1965. 13. Magnusson, B., and Hersle, K.: Patch test methods. II. Regional variations of patch test responses. Acta Dermatovener., 45:257-261,1965. San Mateo Medical Clinic 23 Baldwin Avenue San Mateo, California 94401