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Allergic contact dermatitis in children

Allergic contact dermatitis in children
Literature review current through: May 2024.
This topic last updated: Feb 07, 2024.

INTRODUCTION — Allergic contact dermatitis (ACD) is a delayed-type (type 4) hypersensitivity reaction, which can occur in both children and adults. ACD is due to direct cutaneous contact with an allergen (eg, poison ivy) and presents as a pruritic rash in areas of exposure. Because ACD can mimic other eczematous dermatoses, including atopic dermatitis (AD), diagnosis in children is challenging. Patch testing is the gold standard for the diagnosis of ACD and can be performed in children with a few exceptions. Compared with adults, children have different exposures, and patch testing should be customized to individual patients and their known exposures.

This topic will review the most common allergen exposures, diagnosis, and management of ACD in children. The pathogenesis, clinical manifestation, and management of ACD in adults are discussed separately. Poison ivy dermatitis is also discussed separately. A general review of common allergens in ACD is also presented separately.

(See "Basic mechanisms and pathophysiology of allergic contact dermatitis".)

(See "Clinical features and diagnosis of allergic contact dermatitis".)

(See "Management of allergic contact dermatitis in adults".)

(See "Poison ivy (Toxicodendron) dermatitis".)

(See "Common allergens in allergic contact dermatitis".)

EPIDEMIOLOGY — The estimated prevalence of ACD in children and adolescents is 16.5 percent in one meta-analysis, but it is likely underestimated [1]. This is due to the high prevalence of atopic dermatitis (AD) in children, which can appear clinically similar to ACD, leading to a lower number of children referred for patch testing. According to the American Academy of Dermatology (AAD) Burden of Skin Disease report, contact dermatitis is highly prevalent in the pediatric population [2]. Of 13 million patients who sought medical care for contact dermatitis, 33.5 percent were children aged 0 to 17 years.

Children are patch tested in fewer numbers than adults. In a North American Contact Dermatitis Group (NACDG) analysis of patch testing between 2001 and 2018, only 1871 children were referred for patch testing compared with 41,699 adults during the same period [3], though children make up over 22 percent of the United States population (2020 United States census).

The prevalence of positive patch testing in children is similar to that of adults in the NACDG registry (49.2 versus 52.2 percent, respectively) [3]. In a study using data from the United States Pediatric Allergic Contact Dermatitis Registry from 2018 to 2022 that included 912 children, the prevalence of a positive test to at least one allergen was higher among children with AD compared with children without AD (78.5 versus 70 percent, respectively) [4]. In the European Surveillance System of Contact Allergies network, between 2002 and 2010, 6708 children between the ages of 1 and 16 were patch tested in 11 countries, and 37 percent had a positive patch test [5]. Southeast Asian children 16 years of age or younger patch tested in Singapore between 2007 and 2020 had similar rates of contact dermatitis, with a prevalence of 50 percent [6].

PATHOGENESIS — Initial sensitization occurs when a hapten (allergen) binds with a protein and induces a T cell-mediated response. With repeat exposure, the allergen-specific T cell migrates to the skin, and resulting inflammation leads to dermatitis in the area of contact. Although it was previously felt that children could not develop ACD due to a less mature immune system, studies suggest that ACD in children is likely underrecognized and underdiagnosed [2,7].

The pathophysiology of ACD is discussed in detail separately. (See "Basic mechanisms and pathophysiology of allergic contact dermatitis".)

CLINICAL MANIFESTATIONS

General features — ACD presents with itchy, erythematous, scaly patches and plaques in the area where the skin encountered the potential allergen, such as the earlobes in the setting of ACD to earrings (picture 1) [8]. In children with darkly pigmented skin, erythema may appear dark brown or violaceous instead of pink or red, as typically seen in patients with lightly pigmented skin.

Because the reaction is delayed, it may take several days for the dermatitis to appear after contact. The dermatitis is frequently excoriated.

Acute allergic contact dermatitis – Acute ACD presents with erythema, vesicles or bullae, and edema with serous crusting (eg, poison ivy dermatitis (picture 2B)).

Subacute/chronic allergic contact dermatitis – Subacute or chronic ACD presents with erythema, scaling, and lichenification (eg, foot dermatitis due to rubber in shoes (picture 2A)).

Unique clinical scenarios

Systemic contact dermatitis — While ACD usually occurs after direct cutaneous contact, systemic contact dermatitis occurs when systemic exposure to a contact allergen (through ingestion, intravenous/subcutaneous administration, or inhalation) occurs in an individual previously sensitized to that specific allergen. Systemic contact dermatitis can present as localized dermatitis, such as vesicular hand dermatitis or isolated eyelid dermatitis, or a generalized and diffuse, eczematous eruption (picture 3) [9]. Overall, systemic contact dermatitis is much less common that direct cutaneous contact dermatitis. The most common allergens causing systemic contact dermatitis in children include nickel, cobalt, balsam of Peru, and propylene glycol.

Nickel – Nickel systemic contact dermatitis may present as vesicular hand dermatitis. In one study by the North American Contact Dermatitis Group (NACDG), it was the most common cause of systemic contact dermatitis from oral ingestion of nickel [10]. Potentially high concentrations of nickel can be found in foods, especially beans, peanuts, granola, chocolate, legumes, oatmeal, and soy. There was a report of four kids with nickel systemic contact dermatitis due to ingestion of chocolate eggs during the Easter holiday [11].

Balsam of Peru – Balsam of Peru is a mixture of various fragrance allergens and is a marker of fragrance allergy in children. Systemic ingestion of balsam of Peru can lead to a generalized dermatitis. Common foods high in balsam of Peru include citrus fruit peels, tomato-based products, food flavorings (vanilla, cinnamon, cloves), colas, and certain liquors (eg, vermouth). There are reports of severe systemic contact dermatitis in children due to ingestion of balsam of Peru in tomato ketchup and vanilla-flavored teething biscuits [9,12].

Propylene glycol – Propylene glycol is an emulsifier, preservative, and excipient in various personal care products and topical medicaments, including topical corticosteroids. It is also found in various foods and oral medications. Liquid formulations of common over-the-counter antihistamines, such as cetirizine, diphenhydramine, and loratadine, contain propylene glycol and have been reported to cause systemic contact dermatitis [13]. Propylene glycol is added to prepared foods as a humectant and glazing agent. It is found in prepackaged bread and flour products, desserts and snacks, ice cream, fast foods, and prepared meals, many of which are consumed by children.

Diaper allergic contact dermatitis — Most cases of diaper dermatitis are due to irritant contact dermatitis from bodily fluids, leading to disruption of the acid mantle and maceration of the skin (see "Diaper dermatitis"). However, ACD to diapering products, diaper wipes, and diapers can occur but are likely underrecognized and underreported.

One study found that most diaper creams and wipes contain potentially allergenic ingredients [14]. Topical diaper preparations (eg, barrier creams) contain fragrances, propylene glycol, balsam of Peru, lanolin, and botanical extracts. Similarly, diaper wipes contain propylene glycol, fragrances, botanical extracts, and various preservatives that can potentially lead to ACD.

Components of modern, superabsorbent diapers (including the elastic bands, adhesive strips, color dyes, and added fragrances) can also cause ACD. Elastic bands and cuffs provide a secure fit to prevent leakage from the diaper. Rubber accelerators (eg, mercaptobenzothiazole) and retardants (eg, cyclohexylthiophthalimide) have been implicated as causes of ACD related to diapers [15-17]. Adhesives can be found at the waistline to secure the diaper to the infant. Allergens present within the adhesive, such as p-tert-butylphenol formaldehyde resin [15], have been reported to also cause ACD. This peculiar pattern of diaper ACD, mostly affecting the lateral buttocks and hips (reminiscent of a gun holster), has been termed "Lucky Luke" dermatitis after the Belgian comic cowboy character.

Disperse dyes once popular in diapers have largely been replaced with color pigments in leading diaper brands [18]. Some diapers may continue to use disperse dyes that have been suspected to cause ACD [19], the most common offending color being disperse blue dye. Fragrances may also be added to diapers to impart a refreshing scent.

Toilet seat dermatitis — Children who are potty training or no longer in diapers may be susceptible to toilet seat dermatitis. The dermatitis presents with a "U" shape involving the upper buttocks and extending to the bilateral upper posterior thighs, which are the areas in contact with a toilet seat. Toilet seat dermatitis is more commonly irritant in nature than allergic. Irritant contact dermatitis can be triggered by prolonged sitting on a toilet seat cleaned with a harsh detergent [20]. Wiping the seat with water after cleaning can remove residual chemicals prone to causing irritant dermatitis.

Rarely, toilet seat dermatitis can be allergic. Several cases of toilet seat dermatitis were previously reported to wood varnishes, paints, and to wood itself [21]. Although most toilet seats have transitioned to plastic, these can potentially also cause ACD, although few of these cases have been confirmed with patch testing [22,23].

Site-specific dermatitis — Certain sites of dermatitis in children should prompt consideration for ACD and referral for patch testing.

Hand and foot — Children with chronic hand and foot dermatitis should be patch tested. In a series of 480 children with hand dermatitis [24], 46.8 percent were found to have a positive reaction, with common allergens being nickel, methylisothiazolinone, and fragrances. A study of 82 atopic children with hand and/or foot dermatitis showed positive patch test reactions in one-quarter of patients, with the most common allergens being lanolin and cobalt [25]. Other reported allergens in children with hand eczema include colophony, Compositae mix, and rubber [26]. Rubber allergy should also be considered for children with persistent foot dermatitis [27-29].

Shin — For children with shin dermatitis, patch testing for rubber allergens or plastics that can be found in sports equipment (eg, shin guards) is important. Shin guard dermatitis is typically irritant in nature, however, allergens related to rubber, plastics, and foam intermediates may be implicated. Acetophenone azine, found in ethyl vinyl acetate foam in sports equipment and shoes, is an emerging allergen that has been reported in children and young athletes [30].

Face — Although atopic dermatitis (AD) may commonly involve the face in children, persistence of eyelid dermatitis may suggest allergy, and in a series of 114 patch-tested children, six of seven children with eyelid involvement had positive patch test results [31]. Eyelid and facial dermatitis in children may also represent airborne pattern ACD. Airborne plant ACD (eg, Compositae family) should be considered in cases of recurrent facial and eyelid dermatitis, particularly if there is seasonal variation.

Buttock and thigh — Contact dermatitis involving the posterior aspect of the upper thighs and buttocks may be due to irritants or allergens present on toilet seats (see 'Toilet seat dermatitis' above) or diapering products (see 'Diaper allergic contact dermatitis' above). Although typically irritant in nature, patch testing may be indicated in refractory cases. (See 'Patch testing' below.)

DIAGNOSIS — The diagnosis of ACD is suspected based on the patient's history of allergen exposure and clinical examination. Patch testing is necessary to confirm the diagnosis. An avoidance strategy of common allergens may be tried prior to patch testing [32].

History — A detailed patient history is the first step in determining whether the child has ACD. For the youngest patients, the exposure history is obtained from a parent or caregiver. The clinical history taking is similar to that in adults, and a regional approach to understanding the child's specific exposures is important (see 'Site-specific dermatitis' above). For example, diapering and toileting habits may be particularly important if the patient has diaper or posterior upper thigh dermatitis. Understanding activities and exposures if the child is in daycare or school is frequently relevant. Children with hand dermatitis should be asked about hobbies and recreational activities, including use of toys such as slime, nail products, and games. For older children, an occupational history may be necessary if they have an after-school or weekend job.

Clinical examination — A full skin examination is essential to diagnose ACD in children. While ACD may mimic atopic dermatitis (AD), children may have coexisting ACD and AD. Clinical clues that the patient may have ACD include:

Refractory or treatment-resistant disease.

Lack of seasonal variation.

New-onset rash that is different from the patient's known AD. The distribution of the rash can help in identifying the etiology of ACD. (See 'Site-specific dermatitis' above.)

Skin biopsy — A skin biopsy is not necessary for the diagnosis of ACD, and it is not useful to distinguish ACD from AD, irritant contact dermatitis, or drug eruption, as they share nearly identical histopathologic features. However, if the diagnosis is in question, a skin biopsy can be performed to rule out other skin diseases that may share clinical features with ACD.

Histopathology — The typical histologic finding for ACD is a spongiotic dermatitis. Depending on the acuity of ACD, there may be varying degrees of epidermal edema (more in acute ACD) and acanthosis (more in chronic ACD). Eosinophils may be present, but they are not diagnostic of ACD and do not differentiate among various spongiotic dermatitides [1,33,34]. Langerhans cell microabscesses may be seen but are nonspecific.

Immunohistochemical staining and immunofluorescence are not necessary to ascertain a diagnosis of ACD but may be useful to rule out other etiologies (eg, urticarial-stage bullous pemphigoid and mycosis fungoides) that may present like ACD.

Patch testing — Patch testing is the gold standard for the diagnosis of ACD [35]. (See "Patch testing".)

Patch testing in children is performed similarly as in adults. However, compared with adults, children may experience more anxiety associated with the test, and audio and visual distraction techniques can be used during patch application. The authors routinely use tablet computers in the clinic to distract children during both the placement and removal of patch tests.

Patch testing can be performed in infants if necessary; the authors have patch tested children as young as three months old (picture 4A-B).

Technique – Allergens are applied on the back (picture 5A-B) and left in place for 48 hours. Some groups advocate for patches to be left in place for 24 hours instead of 48 hours [36] to minimize the risk of irritant reactions or strong reactions to allergens such as paraphenylenediamine [37]. However, larger studies of patch testing in children do not show an increased prevalence of irritant reactions in children, and the authors leave patches in place for 48 hours (the same as adults), consistent with published guidelines [38]. Patches may be secured in place with additional cloth tape.

Some groups advocate for the use of plastic instead of aluminum Finn chambers in children because of the risk of contact dermatitis to aluminum in young patients. Children may become sensitized to aluminum from routine childhood vaccinations, as vaccines contain aluminum as an adjuvant [39]. Although rare, aluminum sensitization can lead to numerous positive patch test reactions to the aluminum chambers, confounding the test [40]. The authors test all children with plastic chambers to eliminate the potential risk of aluminum reactivity.

Pediatric series – The allergens chosen for patch testing in children should represent the most common exposures for children. Numerous pediatric baseline series exist, and most represent a truncated version of a standard baseline series used in adults. Allergens on a baseline series that may more likely be occupational in nature, such as epoxy resins or certain acrylates, may not be a relevant exposure for children and can be removed.

Although the thin-layer rapid-use epicutaneous (TRUE) test is the only US Food and Drug Administration (FDA)-approved patch test system for children >6 years of age, this test only contains 35 allergens and frequently can miss common allergens in children (including certain fragrances, surfactants, and preservatives). In 2018, a workgroup of the American Contact Dermatitis Society (ACDS) published a 38-allergen pediatric series [41].

For very young children, the number of allergens is limited by the surface area of the child's back. In these cases, a detailed history of potential exposures is very important, and targeted patch testing to only those ingredients known to be in the patient's exposures is necessary.

Reading – Reading is performed at 48 hours, with additional delayed readings performed between 72 and 144 hours after placement. Certain techniques, such as side lighting for children with darkly pigmented skin, may aid in the interpretation of positive patch test reactions (picture 6).

The reading of patch testing results in children follows guidelines established by the International Contact Dermatitis Research Group [37]:

Extreme reactions (+++) have intense erythema, edema, and vesicles.

Strong reactions (++) have edema, erythema, papules, and occasionally vesicles.

Mild reactions (+) have erythema, edema, and few papules.

Questionable or doubtful reactions (+/-) have faint erythema.

Relevance is determined at the time of the patch test reading, based on the clinical scenario, including the distribution of the child's dermatitis and reported exposures. Of note, the strength of the reaction may not correlate with the clinical relevance. For example, in the setting of facial dermatitis, a mild reaction to a surfactant known to be in the patient's shampoo is more likely to be relevant than an extreme positive reaction to nickel.

Top contact allergens in children — Children have different exposures compared with adults, thereby leading to the different prevalence of top contact allergens. The top 10 allergens in adults and children from the most recent North American Contact Dermatitis Group (NACDG) data are shown in the table (table 1) [3,42].

Nickel — In children, the most common allergen is nickel, a durable, cheap, silver-colored metal commonly used in costume jewelry, belts, jean snaps, keys, and metallic toys. Most cases of nickel allergy are readily identifiable as dermatitis usually occurs over the area of direct contact. Examples are dermatitis of the infraumbilical area due to allergy to nickel in jean snaps or dermatitis of the earlobes for nickel allergy due to earrings (picture 7A-B).

Cobalt — Cobalt allergy is closely related to nickel. Cobalt is also found in costume jewelry, leather, makeup, and blue enamel paints.

Thimerosal — Thimerosal is a mercury-based preservative that was previously used in childhood vaccines but has largely been removed. Most cases of positive patch testing to thimerosal are not relevant due to its rarity in daily products, except for occasional ophthalmic solutions [43,44].

Similar to thimerosal, gold is a frequently positive allergen on patch testing but an infrequently relevant allergen due to generally low exposure in children.

Fragrances — Fragrances are one of the most common allergens in children and can be present in numerous personal care products, including shampoos, deodorants, detergents, sunscreens, and essential oil diffusers [45]. There is no difference in the allergenicity of natural versus synthetic fragrances. A positive reaction is often relevant, and avoidance includes strict elimination of all products with fragrances [46]. Airborne fragrance allergy due to diffusers, sprays, incense, and candles frequently presents on exposed areas of the body, such as the head and neck.

Hydroperoxides of linalool — Linalool is a naturally occurring terpene fragrance that serves as a component of various natural and synthetic fragrances, such as lavender, bergamot, jasmine, and rosewood. Upon contact with air, linalool oxidizes to hydroperoxides of linalool. Linalool is an allergen of significant interest due to its rapidly increasing prevalence in children [47]. There is debate amongst contact dermatitis experts whether linalool is present in high enough concentrations in personal care products to cause ACD upon exposure [48].

Methylisothiazolinone — Preservatives are necessary to prevent bacterial, fungal, and viral contamination of personal care products. Methylisothiazolinone is a water-based preservative in numerous products, including shampoos, conditioners, laundry detergent, hand soap, nail polish, and school glue [49,50]. In the past, methylisothiazolinone has been reported as a contact allergen in wet wipes for children but has since been removed [51]. Children may be exposed to methylisothiazolinone primarily from personal care products as well as arts and crafts. There has been an epidemic of hand dermatitis due to methylisothiazolinone in ingredients used to make slime at home [52]. Methylisothiazolinone (and other isothiazolinones) has also been reported to cause airborne contact dermatitis due to exposure from household and industrial paints [53].

Formaldehyde — Like methylisothiazolinone, formaldehyde is a preservative used in personal care products. Classified as a carcinogen by the US FDA, its market penetration is falling due to consumer and company preference for other preservatives, such as methylisothiazolinone. While formaldehyde is almost never found "as is" in personal care products, formaldehyde releasers, including bronopol, quaternium-15, imidazolidinyl urea, diazolidinyl urea, and dimethylol-dimethyl hydantoin, are labeled in personal care products and must be avoided by patients allergic to formaldehyde.

Neomycin — Neomycin is a common topical antibiotic found in over-the-counter triple antibiotic ointment. It is a frequent contact allergen and can potentially cross-react with systemic aminoglycoside antibiotics. Children who are allergic to neomycin are also frequently allergic to bacitracin, another common over-the-counter antibiotic found in topical double and triple antibiotic ointments.

Prescription mupirocin or retapamulin are safe options for patients with contact dermatitis to bacitracin and/or neomycin.

DIFFERENTIAL DIAGNOSIS — The morphology of ACD is similar to other inflammatory dermatoses that are common in children, including atopic dermatitis (AD), irritant contact dermatitis, psoriasis, and seborrheic dermatitis:

Atopic dermatitis – AD is the most common inflammatory dermatosis in children, most often presenting on flexural areas. Twenty percent of children with AD may have concomitant ACD, and patch testing should be considered in children who do not respond to typical AD treatments or have involvement of unusual locations (eg, hands and feet) [25].

Irritant contact dermatitis – Irritant contact dermatitis may be morphologically similar to ACD. However, irritant contact dermatitis more often presents with stinging; burning; pain; and a history of irritant exposure, such as frequent lip licking, hand washing, or chemical exposure.

Psoriasis – Psoriasis often presents on extensor surfaces and presents with a thick, silvery, micaceous scale that frequently bleeds when traumatized (Auspitz sign).

Seborrheic dermatitis – Seborrheic dermatitis often presents with greasy, yellow scales, most commonly involving the scalp, perinasal folds, postauricular scalp, eyebrows, and central chest in teenagers. Seborrheic dermatitis is uncommon between infancy and prepubertal age children. In neonates and infants, seborrheic dermatitis can involve the intertriginous skin, skin under the diapers, and the scalp (cradle cap).

MANAGEMENT

Allergen avoidance — The mainstay of treatment of ACD in children is avoidance of known allergens. Patients, parents, and caregivers should be counseled on strategies for avoiding allergens. Resources such as the American Contact Dermatitis Society (ACDS) Contact Allergy Management Program (CAMP) can assist with identifying and purchasing products that are safe to use. For example, in cases of suspected ACD to a diaper cream, 100% petrolatum is a hypoallergenic alternative that can be used as barrier ointment. For children with potential ACD to diaper wipes, a soft towel moistened with warm water is an alternative to manufactured diaper wipes.

In most cases, ACD should improve with six to eight weeks of avoidance, but some patients will need up to 16 weeks to fully clear. For dermatitis that does not improve with allergen avoidance:

Reconsider patch test relevance – The relevance of the positive patch test in relation with the clinical manifestations and diagnosis should be reconsidered.

Consider systemic exposure – If patients do not clear with avoidance of allergens, systemic exposures should be considered, particularly for certain allergens (eg, nickel, carmine [a food colorant], other food additives) [54,55]. If children are positive to nickel on patch testing, and there is no obvious source of nickel contact leading to dermatitis, then a low-nickel diet can be considered for a period of four to six weeks to see if there is any improvement [56]. Foods known to be high in nickel content include:

Whole grains (including wheats and oats)

Nuts and seeds

Shellfish

Beans and peas

Chocolate

A low-nickel diet is difficult for patients to follow, and most studies are limited to case reports or series of patients who already notice dermatitis flares with oral nickel intake [54,57]. Recommendations for restrictive diets should be provided with caution, given some restrictive diets may lead to nutritional deficiencies in children.

Pharmacologic treatment — Although allergen avoidance is the mainstay of the management of ACD, pharmacologic treatment is required to achieve rapid control of symptoms in many cases.

Data on the management of ACD in children are limited. Treatment follows the general principles of eczema treatment and includes topical corticosteroids, topical calcineurin inhibitors, topical phosphodiesterase 4 (PDE4) inhibitors, topical Janus kinase (JAK) inhibitors, and systemic immunosuppressive agents.

Limited acute allergic contact dermatitis – For children with limited acute ACD, we suggest topical corticosteroids rather than other topical anti-inflammatory agents as initial therapy. We typically use medium- to high-potency topical corticosteroids (table 2) once or twice daily for up to two to four weeks. In younger children and for the treatment of the face and flexural areas, medium-potency topical corticosteroids can be used for up to two weeks. Topical calcineurin inhibitors, topical JAK inhibitors, and topical PDE4 inhibitors are an alternative to topical corticosteroids for patients who require prolonged treatment (four to six weeks), especially if ACD involves the face and flexural areas, and for patients with documented ACD to topical corticosteroids.

In children over 12 years of age, ruxolitinib is a treatment option, though its use is restricted to less than 20 percent of the body surface area and less than 60 g per week. (See "Treatment of atopic dermatitis (eczema)", section on 'Topical ruxolitinib'.)

Topical crisaborole is another option, especially for very young children, as it is approved for children ≥3 months of age. However, there is a significant proportion of children who complain of burning/stinging upon application, and other listed treatment options may be more efficacious and better tolerated. (See "Treatment of atopic dermatitis (eczema)", section on 'Crisaborole'.)

Severe or widespread acute allergic contact dermatitis – Patients with severe or widespread acute ACD may require systemic immunosuppressant agents. We typically use oral prednisone (at a dose of 1 to 2 mg/kg/day tapered over 14 to 21 days). For example, a regimen that can be used in a 40 kg child with acute and severe poison ivy dermatitis could be 40 mg for seven days, 30 mg for seven days, and 20 mg for seven days.

Subacute/chronic allergic contact dermatitis – Long-term management with topical therapies may be necessary for children with undiagnosed ACD or ACD that is unavoidable due to exposure during sports, work, hobbies, or school. In some cases, systemic therapies may be necessary. Biologics, such as dupilumab, have been used to treat patients with ACD, but the studies are limited, and more data are needed to determine if they are an effective treatment option [58].

PROGNOSIS — There is no cure for ACD other than avoiding identified allergens. Counseling and education of allergens to avoid and providing patients with alternate options is key. In one study, 60 percent of children with relevant patch test allergens showed improvement within 6 to 12 months [59]. If patients do not improve with allergen avoidance, alternative diagnoses should be considered.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Contact dermatitis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Diaper rash (The Basics)" and "Patient education: Poison ivy (The Basics)" and "Patient education: Eczema (atopic dermatitis) (The Basics)")

Beyond the Basics topics (see "Patient education: Contact dermatitis (including latex dermatitis) (Beyond the Basics)" and "Patient education: Diaper rash in infants and children (Beyond the Basics)" and "Patient education: Poison ivy (Beyond the Basics)" and "Patient education: Eczema (atopic dermatitis) (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Clinical presentation – Allergic contact dermatitis (ACD) manifests as an itchy, erythematous, scaly dermatitis, localized over the sites of direct contact with the offending allergen; vesicle and bullae can develop in acute forms (picture 2A-B). ACD typically appears one to three days after exposure, but some reactions may take longer to appear. (See 'Clinical manifestations' above.)

Diagnosis – The diagnosis of ACD is suspected based on a detailed clinical history and physical examination. Particular attention should be paid to sites of dermatitis, such as the hand/foot, face, shin, and diaper areas (see 'Site-specific dermatitis' above). A detailed history should include recreational activities, such as sports or toys, hobbies, toileting, and personal care products (see 'History' above). Patch testing is the gold standard for diagnosis and can be performed even in young children. (See 'Patch testing' above.)

Management

Allergen avoidance – Allergen avoidance is the mainstay of treatment for ACD. Patients and parents/caregivers should be counseled on strategies for avoiding allergens. Resources such as the American Contact Dermatitis Society (ACDS) Contact Allergy Management Program (CAMP) can assist with identifying and purchasing products that are safe to use. In most cases, dermatitis improves with six to eight weeks of avoidance, but up to 16 weeks may be needed for full clearance.

If contact avoidance is not helpful, systemic contact dermatitis due to ingested contact allergens may be suspected. In select cases, a trial of diet low in some potential allergens (eg, nickel, carmine, other food additives) may be attempted. (See 'Allergen avoidance' above.)

Pharmacologic treatment

-Limited acute allergic contact dermatitis – For children with limited acute ACD, we suggest medium- to high-potency topical corticosteroids (table 2) rather than other topical anti-inflammatory agents as initial therapy (Grade 2C). Topical corticosteroids are applied once or twice daily for up to two to four weeks depending on the child's age and area involved. Lower-potency topical corticosteroids are generally used in young children and on sensitive areas (eg, face, intertriginous areas). Topical calcineurin inhibitors are an alternative to topical corticosteroids for patients who require prolonged treatment (>4 weeks), especially if ACD involves the face and flexural areas, and for patients with documented ACD to topical corticosteroids. Topical ruxolitinib may be an alternative option for children ≥12 years of age with ACD involving <20 percent of the body surface area.

-Severe/widespread allergic contact dermatitis – For severe or widespread acute ACD, we suggest a short course of systemic corticosteroids rather than other systemic immunosuppressants (Grade 2C). We typically use oral prednisone at the dose of 1 to 2 mg/kg/day tapered over 14 to 21 days. (See 'Pharmacologic treatment' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges William L Weston, MD, who contributed to earlier versions of this topic review.

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Topic 1731 Version 31.0

References

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