Face dermatitis

Clinical features

• Atopic dermatitis (AD; often referred to by patients as “eczema”) is a chronic inflammatory skin condition characterized by pruritus and pruritic, ill-defined, red, scaly papules and plaques that predominantly affect flexural surfaces (e.g., antecubital fossa, popliteal fossa).

  • The appearance of AD lesions differs based on lesion duration. Chronic lesions are often thickened (i.e., lichenified) from chronic rubbing and excoriated from scratching; acute lesions, on the other hand, can be red and occasionally even weeping.

  • In darker-skinned individuals, long-standing lesions can cause dyspigmentation (either hyperpigmentation or hypopigmentation) that persists after the AD lesion is treated.

• Isolated facial AD is rare except during infancy, in which it is frequently the initial presentation.

  • In infancy, plaques frequently affect the bilateral cheeks which, when the child is able to, they can be observed rubbing.

  • In older children and in adults, facial atopic dermatitis almost always coexists with atopic dermatitis elsewhere on the body.

• In darker-skinned children, facial AD can present as pityriasis alba, which is characterized by scaly, white macules and patches on the face.

• Facial AD frequently becomes secondarily impetiginized (i.e., infected), which presents as acute worsening of eczema with overlying weeping and yellow crusting.

• AD is part of the “atopic triad” with allergic rhinitis and asthma; facial AD may be the heralding sign of this triad in infants.

Differential diagnosis

The differential for facial AD includes irritant contact dermatitis (ICD), allergic contact dermatitis (ACD), seborrheic dermatitis, discoid lupus erythematosus, tinea faciei, and psoriasis.

• Facial dermatitis occurring in the presence of AD elsewhere on the body, with or without the presence of clinical signs suggestive of atopy (e.g., nasal crease, allergic shiners), suggests a diagnosis of facial AD.

• Isolated facial dermatitis in adults is unlikely to be AD in the absence of a history of known AD.

• AD often occurs in an overlap state with components of ICD and ACD.

  • Patients with known AD or other facial dermatitis who are treated with topical corticosteroids may also develop steroid-induced rosacea.

  • Topical corticosteroid withdrawal from overuse and discontinuation may mimic an AD flare.

  • Identifying concomitant ACD is important because topical therapy alone is unlikely to be adequate in this setting unless identification of the allergen and avoidance occurs.

• Facial ICD can occur anywhere on the face but most frequently presents in the nasolabial folds and periocular areas because irritants frequently collect into these concave areas.

  • The presence of peeling skin suggests a component of ICD.

  • ICD is common in the winter in arid climates and most frequently occurs in individuals who use harsh facial cleansers and other cosmetics.

    • A subset of facial AD can be seen in acne patients who are using irritating topical therapies (e.g., tretinoin, benzoyl peroxide).

  • AD can be distinguished from ICD in that facial AD frequently coexists with AD present elsewhere. Nevertheless, many patients with facial AD have a component of ICD.

• ACD can be clinically indistinguishable from facial AD; however, a diagnosis of ACD is suggested in adults with no history of AD who develop acute to subacute facial dermatitis.

  • ACD should be suspected in patients with new, persistent facial dermatitis despite treatment with topical corticosteroids.

  • Several distinct patterns of facial ACD are discussed in Chapter 3 . Identification of these patterns can help distinguish ACD from AD.

• Seborrheic dermatitis can typically be distinguished from AD because seborrheic dermatitis: 1) predominantly affects seborrheic areas such as the nasolabial folds, eyebrows, scalp, ears, and retroauricular area and 2) typically has greasy-appearing, overlying scale.

• Tinea faciei can typically be distinguished from atopic dermatitis because it is usually unilateral and frequently has central clearing. Additionally, gentle scraping of tinea faciei lesions with a microscope slide will produce large amounts of micaceous scale that can be examined under the microscope with KOH stains, revealing hyphae.

• Discoid lupus can be distinguished from AD because discoid lupus is almost never itchy and is morphologically distinct with rough peripheral scale and central scarring.

• Psoriasis is infrequent on the face and is usually associated with psoriasis elsewhere, such as the scalp, elbows, and knees. The lesions are erythematous with silvery scaling and sharply circumscribed. Unlike with tinea, the KOH scraping would be negative.

Work-up

• A total-body skin examination should be performed to look for characteristic skin lesions elsewhere.

• A histopathologic confirmation is almost never necessary.

• Patch testing adults with facial dermatitis is indicated when obvious triggers cannot be identified based on history alone and when topical therapy is inadequate for disease management.

Initial steps in management

• Initial management of atopic dermatitis involves a three-pronged approach:

  • Dry skin care, including:

    • Barrier repair with noncomedogenic (which means it does not cause acne; this is listed on product labels) moisturizing creams at least twice daily.

      • For facial dermatoses, it is frequently helpful to recommend a lighter, more cosmetically acceptable moisturizer for morning application (e.g., Neutrogena Hydro Boost gel cream, CeraVe lotion, Eucerin lotion) and a thicker, more hydrating moisturizer for evening application (e.g., CeraVe moisturizing cream, Eucerin cream).

      • In patients without suspected ACD, morning facial moisturizers should routinely contain a sunscreen (e.g., Neutrogena Hydro Boost City Shield, CeraVe AM, Eucerin Daily Protection).

    • A gentle cleansing of the face with water and with or without a gentle cleanser to remove environmental allergens should be performed twice daily every day (morning and evening). The patient’s washed hands should be used rather than a washcloth. Face washing should always be followed immediately by moisturizing.

      • Patients with active dermatitis should be counseled to avoid using exfoliating face washes, such as those containing salicylic acid, glycolic acid, or alpha hydroxy acid.

  • Topical antiinflammatory agents:

    • First-line treatment should include a low-potency topical corticosteroid, such as hydrocortisone 2.5% cream, applied twice daily.

      • Even low-potency topical steroids should be avoided on the eyelids if prolonged use is anticipated.

      • Topical steroids around the eyes can precipitate glaucoma in susceptible patients and therefore should be used with caution or avoided and substituted with a noninflammatory steroid, such as a topical tacrolimus product (tacrolimus or Protopic ointment) or a topical pimecrolimus cream (pimecrolimus or Elidel cream).

      • On the face, all topical steroids can trigger perioral dermatitis/steroid rosacea.

        • In both of these settings, use a topical calcineurin inhibitor, such as tacrolimus or pimecrolimus, 0.1% twice daily. Note that this treatment is not recommended by the U.S. Food and Drug Administration (FDA) in infants and in children 2 to 15 years of age; instead, tacrolimus 0.03% is FDA endorsed.

        • Another steroid-sparing alternative, crisaborole (commercially available as Eucrisa), is a phosphodiesterase-4 inhibitor and is available as an ointment for the use of AD in patients older than 2 years of age.

    • The maintenance of control in patients with relapsing disease that cannot be adequately maintained with dry skin care alone can be performed using topical calcineurin inhibitors, such as topical pimecrolimus 0.1%, twice daily.

      • Some patients require a maintenance application of topical calcineurin inhibitors three times weekly in the absence of active disease to prevent flares.

      • Topical pimecrolimus should not be applied to actively inflamed skin because it can cause a severe burning sensation.

      • Topical tacrolimus and crisaborole only come in ointment form and are often not acceptable cosmetically for daily facial application.

  • Trigger avoidance:

    • Questioning patients with facial dermatitis about their daily facial skin care regimen should occur at every visit for facial dermatitis because facial cosmetics and cosmetic removers can worsen AD and cause ICD and ACD.

      • Patients with refractory facial dermatitis often benefit from complete discontinuation of all cosmetics (facial and otherwise) for at least 4 weeks while actively treating the patient with antiinflammatory topicals. This includes nail polish/acrylic nails that are often found to be the allergic culprit, especially for eyelid or periocular dermatitis.

      • Patients with persistent disease despite discontinuation of cosmetics frequently benefit from patch testing.

Warning signs/common pitfalls

The biggest pitfall when managing AD in any location is failure to promote patient adherence to a dry skin care management regimen. Such a regimen is essential for achieving and maintaining disease control in patients with AD; failure to implement a daily dry skin care regimen ensures treatment failure.

• Patients must specifically be counseled that twice- daily use of their prescription topical antiinflammatory is not a substitute for frequent moisturization.

• Avoidance of harsh soaps and irritating cosmetics/perfumes is essential. Patients need specific product recommendations because the cosmetic aisle in drug stores is otherwise confusing and the internet is full of misinformation on this subject.

Patients with facial dermatitis are frequently noncompliant with therapy if topical medications with poor cosmesis (e.g., ointments) are prescribed.

• If patients are unwilling to use a topical corticosteroid or topical calcineurin inhibitor in the morning because of unacceptable cosmesis, use of a stronger ointment for nightly use only can be considered (e.g., tacrolimus 0.1%, hydrocortisone 2.5% ointment) as long as the patient is counseled extensively about the potential adverse effects of more potent therapies.

• Avoidance of fluorinated topical steroids on the face (topical steroids listed in classes I, II, and III) should be adhered to because these can cause significant adverse effects if used chronically, especially on the thinner skin of the face.

• Noncompliance with moisturizers can occur for similar reasons as noncompliance with therapy.

Failure to identify coexisting dermatoses such as ICD to cosmetics, ACD (including to topical corticosteroids), and/or head and neck dermatitis can interfere with successful management.

• Most patients should be able to achieve disease control with appropriate topical therapies. Coexisting diagnoses should be considered in patients who fail to improve.

Counseling

You have atopic dermatitis, also known as “eczema.” Atopic dermatitis is usually an inherited chronic skin condition (meaning there is no cure) that occurs in people who have skin that does not retain enough water and that does not adequately protect itself against outside allergens. Your skin is sensitive, prone to dryness, and susceptible to becoming itchy and developing rashes.

Individuals with atopic dermatitis develop skin inflammation from within in response to the environment around them. This inflammation makes the skin red and itchy. Importantly, there is no one allergen that causes your skin disease. Additionally, dietary changes have not been reported in the medical literature as curing your disease.

Treating your skin disease requires that you keep your skin healthy by moisturizing it and by avoiding exposure to things that irritate it. To keep your skin healthy, it is important that you wash your face with a gentle cleanser twice daily using your hands instead of a washcloth. After cleansing your face, you should immediately apply a moisturizer. Some people find it helpful to use a different, lighter moisturizing cream (such as a lotion or light cream) in the morning than the one they use at night because the heavy moisturizers (heavy creams or ointments) that are better for keeping the skin hydrated (e.g., CeraVe moisturizing cream or Eucerin Advanced Repair cream) may not be cosmetically suitable for use during the daytime. While your skin is still red and irritated, it is important that you do not apply any cosmetics or fragrances because these can inflame or irritate your skin.

Your doctor has prescribed you a topical mild steroid cream. You should use this cream twice daily only for 7 to 10 days, at which time the redness and irritation should be gone. Alternative steroid-sparing creams may also be prescribed for more chronic or intermittent use.

These prescription creams are not a substitute for your moisturizer and should be used with your moisturizer, not instead of your moisturizer. Once the redness and irritation has resolved, you can stop the prescription cream, although you may need to restart it if the redness and irritation return. The topical steroid prescribed cream can cause side effects if you use it too frequently or if you use it for too long. This includes possible thinning of the skin, increased visibility of blood vessels in the area of application, discoloration of the skin, and potentially an acnelike rash. Additionally, if this cream is applied around the eye it can cause an increase in eye pressure, which can result in glaucoma, a vision-threatening eye disease. Please tell your doctor if you have a personal or family history of glaucoma.

Atopic dermatitis is cyclical, which means you will have times when your rash is much better and times when it is much worse. Different people flare for different reasons. You should try your best to identify things that are unique triggers for your atopic dermatitis. You will have to work with your doctor over time to find a skin care regimen that is right for you and that keeps your skin disease under control.

Clinical features

• Seborrheic dermatitis of the face may affect the nasofacial junction, eyebrows, hairline (extending onto the scalp as discussed in Chapter 1 ), retroauricular area, and, less frequently, the chin.

  • Identifying whether a rash presents with a seborrheic distribution is essential for diagnosing seborrheic dermatitis, especially in subtler cases characterized by barely perceptible pink plaques, pruritus, and mild flaking.

  • Seborrheic distribution is associated with hair-bearing and oily areas of the head, including the scalp, forehead, eyebrows, eyelash line, nasolabial folds, beard area, postauricular area, and submental skin.

• Seborrheic dermatitis is characterized by the development of pink-red thin patches or plaques with overlying greasy, thick scales.

  • Presentation can range from pruritus and a barely perceptible rash to deep red plaques encroaching past the classic seborrheic distribution.

• Isolated facial seborrheic dermatitis is relatively uncommon. In most cases, dandruff or scalp involvement can be appreciated, regardless of disease severity elsewhere.

Differential diagnosis

The differential for facial seborrheic dermatitis includes psoriasis, ICD, acute cutaneous lupus erythematosus, ACD, Darier disease, rosacea, and, rarely, drug reactions.

• Psoriasis is uncommon on the face and, when present, is usually associated with psoriasis elsewhere on the skin. Psoriasis on the scalp, however, is common. Psoriasis usually has silvery scaling and the lesions are well demarcated. The lesions of seborrheic dermatitis are generally not as sharply demarcated and are greasier in appearance with more yellowish scales. It is not uncommon for patients to have both conditions.

• ICD, typically arising from personal care product use or from irritating topical medications for acne (e.g., benzoyl peroxide, tretinoin) mimics seborrheic dermatitis by creating “dermatitis” (manifesting as redness and scaling) at the nasofacial junction (specifically at the alar-facial crease). This so-called “dermatitis” develops because the concavity of the alar-facial crease promotes accumulation of irritating cosmetics and topical medications within the area. This area may develop ICD from topically applied products in the absence of ICD elsewhere.

  • Obtaining a facial skincare regimen history in all patients presenting with a facial rash is a priority and can help differentiate ICD from seborrheic dermatitis.

    • Importantly, seborrheic dermatitis and ICD can occur in an overlap state where underlying seborrheic dermatitis is exacerbated by use of irritating topicals.

  • The presence of rash in nonseborrheic areas, especially concave areas with thin skin such as the periorbital area, suggests a diagnosis of ICD over seborrheic dermatitis; on the other hand, the presence of rash in other classic seborrheic areas (e.g., on the hairline) is suggestive of seborrheic dermatitis.

• Severe seborrheic dermatitis is often misdiagnosed as acute cutaneous lupus because seborrheic dermatitis can mimic a malar rash.

  • Unlike seborrheic dermatitis, which favors the alar-facial crease, acute cutaneous lupus characteristically spares this area because it is sun protected.

• ACD does not typically conform to a typical seborrheic distribution, even though plaques on the cheeks occurring in both diseases may look similar.

• Darier disease can look almost indistinguishable from seborrheic dermatitis; however, disease severity, nail changes, family history of Darier, treatment refractoriness, and the presence of disease elsewhere should all suggest a diagnosis of Darier.

• Rosacea is another cause of red cheeks; however, it typically spares the alar-facial crease and lacks overlying scale; rosacea is also often seen in association with acneiform papules, pustules, and telangiectasia.

Work-up

• A total-body skin examination should be performed to look for characteristic skin lesions elsewhere.

• Asking a patient about their daily facial skincare regimen is essential for distinguishing facial seborrheic dermatitis from ICD and for assessing for overlap of the two conditions.

• Adults who present with subacute onset severe seborrheic dermatitis affecting the face and chest should be screened for human immunodeficiency virus (HIV) unless another obvious trigger for development of seborrheic dermatitis is identified (e.g., organ transplant immunosuppression, Parkinson disease).

• Seborrheic dermatitis is generally a clinical diagnosis; rarely is a biopsy required to make a diagnosis of seborrheic dermatitis.

Initial steps in management

There is no cure for seborrheic dermatitis. The course is chronic with waxing and waning. Failure to emphasize the importance of using a maintenance therapy virtually guarantees disease recurrence and patient dissatisfaction.

Treatments for seborrheic dermatitis are primarily divided into topical antifungals and topical antiinflammatory agents.

Warning signs/common pitfalls

Consider a patient’s bathing habits when treating seborrheic dermatitis because infrequent bathing and infrequent shampooing are a common cause of treatment failure/nonadherence to medicated shampoos.

There is no cure for seborrheic dermatitis; therefore, all patients require maintenance treatment.

For facial seborrheic dermatitis, cream formulations are preferable over ointments because they are typically more cosmetically acceptable.

Failure to identify concomitant personal care product-induced ICD can hinder patient improvement despite appropriate treatment.

Patients with acute onset of severe seborrheic dermatitis should undergo HIV testing.

Patients using antifungal shampoos should alternate daily between different types of shampoos to decrease the likelihood of secondary treatment failure.

Counseling

You have a rash called “seborrheic dermatitis.” It is a severe form of dandruff that can involve the face and also the scalp and chest. This is a chronic, recurrent, waxing and waning type of rash, meaning that there is no cure. Most importantly, it is a self-limited type of rash, meaning that it will not cause you internal harm. This rash is the result of inflammation caused by your immune system. The exact reason that you have developed this rash is unknown. Some experts think that it develops because your immune system overreacts to fats made by a yeast called “ Malassezia ” that lives on your skin; however, other experts do not think this is the case. Because this is a normal skin yeast, it is not a form of infection and is not contagious.

I have prescribed you an antifungal (yeast) shampoo. You should use this shampoo 3 times per week for 4 weeks. You should apply it to your face and your scalp. You do not need another facewash while using this shampoo. It is important that you let the shampoo remain on your skin for at least 5 minutes before rinsing it out. In 4 weeks, you can decrease the frequency with which you use this shampoo to once per week. It is important that you continue to use this shampoo once every week because if you do not, it is likely that the rash will come back. On the days that you do not use the antifungal shampoo, I recommend that you use an over-the-counter shampoo containing either selenium sulfide or zinc pyrithione because these products also have antifungal properties. Examples of brands that contain these ingredients include Selsun Blue and Head & Shoulders. If one of these shampoos that you have been using chronically loses its effectiveness, switch to another type of shampoo; always use at least two different types of shampoos during the week to reduce this possibility.

Clinical features

Allergic contact dermatitis (ACD) of the face is a delayed hypersensitivity reaction to immunogenic agents, classically soaps, shampoos, hair dyes, cosmetic agents, and nail polish. The face is one of the most common sites for development of ACD.

Common geographic pattern:

• Acute ACD generally presents as pruritic and eczematous plaques, whereas chronic ACD that develops from prolonged allergen exposure classically takes on a lichenified and scaly appearance.

• The rash is normally localized to the specific regions of allergen exposure; however, the overall pattern of facial involvement can be helpful in distinguishing the most likely causal allergen.

  • Involvement of the face that is localized to the lateral neck, preauricular, and temporal regions may be because of allergens applied to the scalp (e.g., hair dyes, shampoos) that rinse off and spread to the face.

  • Lesions that are patchy and develop on the bilateral cheeks may be driven by exposure to cosmetic agents, including moisturizers, fragrances, and sunscreens.

  • Lesions on the upper eyelids ( Fig. 2.1 ) may be the direct result of eye makeup, metal in makeup applicators, or eyelash curlers or may occur indirectly from nail polish exposure when scratching one’s eyes.

    • Upper eyelid involvement (“headlight sign”) can also be because of airborne contact dermatitis, which classically results from reactivity against specific plants pollens (e.g., ragweed, sunflowers) or occupational exposures (e.g., fiberglass, resins, nickel, wood dust).

      • In these cases, skin involvement may also involve other regions readily exposed to pollen allergens, including the upper chest, neck, and submandibular region.

    

• The development of ACD on the face involves a sensitization phase of 10 to 14 days after initial exposure.

  • Upon subsequent exposure, dermatitis may appear within 12 to 48 hours.

  • Repeated exposures to the allergen can lead to chronic disease, in which the skin becomes thickened, lichenified, and hyperpigmented.

  • Daily exposure is not required to maintain a reaction.

Differential diagnosis

The major differential diagnoses for facial ACD include ICD, AD, seborrheic dermatitis, and phototoxic drug reactions.

• ICD is particularly difficult to distinguish from facial ACD because both follow exposure to a contactant; however, ICD commonly exhibits better demarcation than ACD.

  • Patch testing may be of particular value in these cases; however, ACD/ICD overlap is common and withdrawal of the contactant is a priori in ACD, ICD, and ACD/ICD overlap.

• AD develops in individuals with a personal history of eczema, asthma, or allergic rhinitis at a young age. Isolated facial AD would be unusual. AD typically presents symmetrically in a flexural distribution (antecubital fossae, popliteal fossae, etc.).

• Seborrheic dermatitis can be distinguished from AD because: 1) it typically localizes into a seborrheic distribution (i.e., it affects the nasolabial folds, eyebrows, retroauricular area, and scalp) and 2) it has overlying, greasy-appearing scale.

• A phototoxic drug reaction presents as an exaggerated sunburn in sun-exposed regions, including the face, but patients classically have a history of using specific medications (e.g., tetracyclines, fluoro-quinolones, nonsteroidal antiinflammatory drugs [NSAIDs], hydrochlorothiazide).

Work-up

Clinical presentation, history, and, in chronic cases, patch testing help establish a diagnosis of facial ACD.

• A total-body skin examination is recommended to identify the presence of a characteristic ACD rash that is localized to the regions previously described.

  • A total-body skin examination is helpful for ruling out other causes of eczematous facial dermatitis, such as AD, because rash elsewhere would be expected in these cases.

• Patient history should be targeted toward identifying a prior history of similar events in addition to evaluating for any new exposures to potential allergens.

  • Classic allergens causing ACD from direct facial contact include cosmetics and lotions with fragrances.

  • Classic facial allergens that impact the face after scalp rinse-off include hair dyes, perming solutions, shampoos, soaps, and topical medications (especially minoxidil).

  • The most frequent causes of facial ACD from indirect hand contact are nail polishes and hand lotions.

  • Exposure to specific pollens or workplace allergens (e.g., fiberglass, resins, nickel, wood dust) may be suggestive of airborne contact dermatitis.

  • A patient history of AD (asthma, hay fever, conjunctivitis) increases the risk for future development of ACD.

• If an offending agent is strongly suspected, it can be useful for the patient to avoid this agent and see if the symptoms resolve or improve.

  • If a particular product is not strongly suspected, however, it is impractical and not recommended to blindly remove potential allergens because many products share similar allergens and this does not frequently lead to identification of the allergen.

  • Instead, in these situations, a “cosmetic holiday,” as it is colloquially known, may be recommended to broadly identify the class of allergen exposure.

• For a patient presenting with new-onset facial ACD that is extensive or involves sensitive areas (e.g., the eyelids), it is recommended to refer the patient to a dermatologist for further management and patch testing.

  • Referral to a dermatologist for patch testing can also be pursued if the offending allergen cannot be easily identified or if the patient demonstrates persistent features of ACD.

  • Note that patch testing is different from prick testing, which is an alternative allergy test performed by an allergist.

  • Despite some patients believing that certain foods are causing their ACD, foods are a rare trigger and are more likely to cause a widespread reaction (systemic contact dermatitis) that is not localized to specific skin regions.

Initial steps in management

General management comments:

• The treatment approach for a patient with suspected ACD of the face is targeted toward removing the offending agent (if identified), protecting the skin, and providing treatments to reduce skin inflammation and patient symptoms.

The recommended initial treatment approach for acute ACD of the face involves multiple steps.

• Patients should be informed of common allergen-containing products that can cause ACD of the face.

  • If the trigger is easy to identify, the importance of allergen removal should be emphasized.

  • Patients should be advised to further reference manufacturer sites to identify specific allergens in household items.

• Emollients (e.g., Vaseline, Aquaphor) can be applied to the affected regions to provide a protective barrier against potential allergens.

• To reduce skin inflammation, we recommend the use of moderate-potency topical corticosteroids (fluocinolone acetonide 0.01% cream, triamcinolone acetonide cream 0.1%) twice daily for 2 to 4 weeks on the affected skin areas.

  • Patients with ACD of the hair-bearing scalp may benefit from high-potency corticosteroids (clobetasol propionate 0.05% solution or fluocinonide acetate 0.05% solution) nightly ( Chapter 1 )

• If immediate reduction in skin inflammation is desired, or if facial involvement is extensive, a 20-day course of oral corticosteroids (e.g., prednisone) is suggested alongside referral to a dermatologist.

  • Dosing should be weight adjusted at a rate of 1 mg/kg.

  • A typical 20-day taper of oral prednisone for an average-weight patient would involve 40 mg daily for 5 days, 30 mg daily for 5 days, 20 mg daily for 5 days, and 10 mg daily for 5 days, with all doses taken in the morning.

  • Shorter, 5- to 7-day doses typically result in rebound flaring after cessation.

  • Systemic comorbidities, such as heart failure, glaucoma, poorly controlled hypertension, and diabetes mellitus should be taken into account when prescribing oral corticosteroids.

What to do if there is a partial but inadequate response after a 4-week trial of topical corticosteroid monotherapy:

• Confirm patient compliance with the treatment regimen and address any compliance barriers.

• Reconsider the diagnosis of ACD or consider other potential allergens.

• Refer patient to a dermatologist for definitive management (patch testing).

Warning signs/common pitfalls

• Although patients may attribute new rashes to the use of specific products, it is essential to judge the feasibility of these explanations (i.e., if there is a temporal and geographic relationship between product use and rash development).

• Patients with extensive facial involvement or involvement of particularly sensitive areas, such as the eyelids, are unlikely to be adequately treated with topical steroids.

  • In these cases, oral corticosteroids and a referral to a dermatologist for further management are recommended.

• Prick testing is not equivalent to patch testing and is not suitable for identifying allergens causing ACD.

Counseling

The rash on your cheeks is caused by allergic contact dermatitis, a skin reaction that develops when your immune system reacts to a product, chemical, or medication in your environment. This rash can be bothersome and itchy but is typically not dangerous and can be controlled with medications.

There are a few ways that we manage this rash. First, we want to identify any potential triggers in your day-to-day life. Classic triggers that cause this rash to develop on the face include fragrances, moisturizers, and lotions. You may want to avoid using any skin products that you may have come in contact with recently. If you do not strongly suspect a particular product, however, we do not recommend that you avoid exposing yourself to a number of daily products because this is not usually helpful. In the meantime, we have prescribed you a topical steroid cream to control the rash. You should apply this twice daily on the affected areas of your face for 2 to 4 weeks. Most people tolerate this well over a short period of time, although some say that it causes their blood vessels underneath their skin to become slightly more noticeable. Most patients begin to see their rash resolve within 2 to 4 weeks of consistently using the cream. Some patients also find it helpful to use moisturizers, such as Aquaphor, on their face to protect their skin from further allergen contact.

If your rash continues after these treatments, you may be a candidate for a special type of testing to help us identify the product causing your symptoms. This is called “patch testing,” and it is a painless test performed in a dermatologist’s office. During this test, many different allergens are placed on your back and secured with tape. They are kept there for 2 days, after which point they are evaluated to determine if you are allergic to any of the agents. This is often helpful in identifying the cause of the rash; however, it can also sometimes identify products that are not causing your immediate problem.

Clinical features

Irritant contact dermatitis (ICD) is caused by physical, chemical, or mechanical damage to the skin and it is a common cause of facial dermatitis.

• Facial ICD can be broadly subdivided into three types. All subtypes present with a red, scaling eruption that may become lichenified and result in dyspigmentation if left untreated.

  • Diffuse/spotty—This is the most common subtype of facial ICD. It is characterized by the development of a red and scaly eruption of the cheeks, forehead, and chin. Although the nose can be affected by ICD, it is involved less frequently than other areas because the nose’s thick skin and plethora of sebaceous glands are protective against irritants.

    • Diffuse/spotty ICD most commonly develops from personal care products; however, gardeners and lawncare workers may develop this from aerosolized pesticides and other lawncare products; housekeepers may also develop this from aerosolized household cleansing products.

  • Periorbital—This subtype of ICD can present with isolated upper or lower lid dermatitis, or it can present with involvement of both. Upper versus lower lid involvement is caused by different inciting agents (e.g., eye shadow for upper eyelid, eye drops for lower eyelid).

  • Lips—Distinct from perioral dermatitis, a steroid-induced and rosacea-like eruption, lip dermatitis is characterized by cheilitis with or without perioral erythematous plaques. One notable subtype of lip ICD is lip licker dermatitis, a common pediatric dermatosis, where cheilitis and perioral eczematous plaques arise from chronic lip licking. Similarly, infants may have lip/perioral ICD from drooling.

• The biggest cause of both facial ICD and facial ACD is personal care products and their applicators. Contrary to popular belief, this is true in both men and women.

• Personal care products that are applied to the hair may drip onto the face and neck and cause ICD.

• Isolated facial ICD in the absence of dermatitis elsewhere on the body is very common, especially in cases where facial ICD arises from the application of facial cosmetics.

• Facial ICD is more common in patients with underlying AD because their underlying skin barrier impairment predisposes them to ICD.

Differential diagnosis

The differential for facial ICD includes ACD, photodrug reaction, AD, seborrheic dermatitis, rosacea, perioral dermatitis, and angular cheilitis.

• ACD is often clinically indistinguishable from ICD. This is further complicated by the fact that personal care products, the most common cause of facial ICD, are also the most common cause of facial ACD.

  • A combination of the withdrawal of offending agents, repair of the skin barrier, and use of topical antiinflammatories is the treatment of choice for both ACD and ICD.

    • Cases of presumed ICD that fail to respond to treatment or in which an offending agent is not easily identified may benefit from patch testing as outlined in Facial ACD.

• Photodrug reactions can mimic acute, diffuse facial ICD ( Fig. 2.2 ). The sparing of photospared areas (e.g., the nasolabial crease, upper eyelid, and submental area) is supportive of a diagnosis of a photodrug reaction, as is a history of recent initiation of a photosensitizing medication (e.g., doxycycline, hydrochlorothiazide).

  

• AD can affect the eyelids, face, and flexural neck. This typically occurs in more severe cases and is almost always accompanied by AD elsewhere on the body (e.g., popliteal fossa, antecubital fossa).

  • ICD occurs more commonly in individuals with AD; therefore presence of AD elsewhere on the body does not rule out a diagnosis of facial ICD.

• Seborrheic dermatitis frequently affects the nasolabial folds, eyebrows, hairline, and beard area. Its distribution and overlying greasy scale frequently distinguish it from ICD.

  • ICD also frequently affects the nasolabial fold as irritating cosmetics accumulate within this concave area. In these cases, ICD may also be identified in the concave periocular area.

• Rosacea may present with redness of the cheeks and nose and superimposed papulopustules; however, it is unlikely to be itchy and is typically associated with telangiectasias.

• Perioral (or periorificial) dermatitis is a misnomer. It is not a true dermatitis. It looks like papulopustular rosacea; however, it concentrates around the mouth and sometimes the eyes and can occur spontaneously or be caused by chronic corticosteroid use. Inhaled corticosteroids are a common, often overlooked culprit. Rarely, topical calcineurin inhibitors can cause perioral dermatitis.

  • Lip ICD can be distinguished from perioral dermatitis because it is a true dermatitis and also frequently coexists with cheilitis.

Work-up

All patients with facial ICD need to be asked about their facial skincare regimen, including the use of prescription topical medications and eye drops.

A total-body skin examination should be performed to look for characteristic skin lesions of other diagnoses in the differential.

ICD is generally a clinical diagnosis and rarely is a biopsy required to make the diagnosis.

Patients who fail to improve after the withdrawal of possible offending agents and the use of topical treatment should be offered patch testing.

Initial steps in management

All patients with facial ICD require:

• Withdrawal of the suspected irritant

  • Changing from one brand of personal care product (e.g., mascara) to another does not always improve facial ICD because many products contain similar ingredients.

• For facial dermatoses, it is frequently helpful to recommend lubrication and facial washing twice a day. A lighter, more cosmetically acceptable moisturizer for morning application (e.g., Neutrogena Hydro Boost gel cream, CeraVe lotion, Eucerin lotion) and a thicker, more hydrating moisturizer for evening application (e.g., CeraVe moisturizing cream, Eucerin cream) may enhance patient compliance.

  • In patients without suspected ACD, morning facial moisturizers should routinely contain a sunscreen (e.g., Neutrogena Hydro Boost City Shield, CeraVe AM face, Eucerin daily protection).

  • Patients with significant skin irritation may experience burning with moisturizer application because of preservatives within the moisturizer.

  • Gentle cleansing of the face with water and with or without a gentle cleanser to remove environmental allergens should be performed twice daily every day (morning and evening). The patient’s washed hands should be used rather than a washcloth. Face washing should always be followed immediately by moisturizing.

    • Patients with active dermatitis should be counseled to avoid using exfoliating face washes such as those containing salicylic acid, glycolic acid, or alpha hydroxy acid.

    • A topical antiinflammatory

  • First-line treatment should include a course of a low-potency topical corticosteroid, such as hydrocortisone 2.5% cream, applied twice daily.

    • Even low-potency topical steroids should be avoided on the eyelids because they can precipitate glaucoma in susceptible patients and are prone to cause steroid atrophy of this thin skin.

    • On the face, all topical steroids can trigger perioral dermatitis/steroid rosacea.

      • In both of these settings, use a topical calcineurin inhibitor, such as pimecrolimus 0.1%, twice daily.

        • Topical pimecrolimus should not be applied to actively inflamed skin because it can cause a severe burning sensation.

    • Topical tacrolimus and crisaborole only come in an ointment and are often not cosmetically acceptable for daily facial application.

      • In contradistinction, ointments are usually preferable for irritant cheilitis.

Warning signs/common pitfalls

The biggest pitfall when managing facial ICD is failure to withdraw the offending irritant. Chronic use of topical corticosteroids is not a substitute for this step of the management process.

• In scenarios where patients are applying multiple personal care products to the affected area(s), withdrawal of all agents should be considered. After resolution of the rash, products can be added back one at a time as tolerated. Initial introduction of a product should be to a limited portion of the skin, such as behind or under the ear, so that if the culprit is identified, a recurrence of a full facial flare is avoided.

• Failure to promote a dry skin care regimen increases the likelihood of ICD relapse after successful treatment.

• Patients must specifically be counseled that twice- daily use of their prescription topical antiinflammatory is not a substitute for frequent moisturization.

Patients with facial dermatitis are frequently noncompliant with therapy if topical medications with poor cosmesis (e.g., ointments) are prescribed.

• If patients are unwilling to use a topical corticosteroid or topical calcineurin inhibitor in the morning because of unacceptable cosmesis, use of a stronger ointment for nightly use can be considered (e.g., tacrolimus 0.1%, triamcinolone 0.1%) for a limited duration and as long as the patient is counseled extensively about the potential adverse effects of more potent therapies.

• Noncompliance with moisturizers can occur for similar reasons as stated above.

Failure to identify coexisting dermatoses such as ACD (including to topical corticosteroids), AD, and/or seborrheic dermatitis can interfere with successful management.

The chronic use of topical corticosteroids on the face, even low-potency topical corticosteroids, can cause skin atrophy, induce an acneiform eruption, what is colloquially known as “red face syndrome,” a type of topical steroid addiction in which patients flare after the discontinuation of topicals.

• If red face syndrome is suspected, consider weaning the patient off of topical corticosteroids with diminishing strengths and frequency of use of topical steroids and then a topical calcineurin inhibitor.