Eyelid Dermatitis (xeroderma of the eyelids, eczema of the eyelids, atopic dermatitis, allergic contact dermatitis, irritant contact dermatitis, seborrheic dermatitis of the eyelids)

Are You Confident of the Diagnosis?

Eyelid dermatitis is an umbrella term describing a group of inflammatory skin disorders that localize to the eyelids and resemble eczema. There are many causes of eyelid dermatitis, hence it is a vexing problem for patients and can represent a diagnostic and therapeutic dilemma. Knowledge of the common causes and their key features can focus the history and physical examination and alert the clinician to more serious conditions.

Time course, patient age, symptoms, presence or absence of scale or edema, distribution (isolated lesion vs multiple, discreet vs diffuse, bilateral vs unilateral, lid margin vs crease) help differentiate the different types of eyelid dermatitis. This chapter reviews the common periorbital dermatoses with emphasis on their distinguishing features.

Most common causes of eyelid dermatitis are

–Contact dermatitis (allergic and irritant), 50% to 76% of cases

–Atopic dermatitis, 12% to 17%

–Seborrheic dermatitis 8% to 16%

–Rosacea, less than 5%

There are other conditions of the eyelids that mimic eyelid dermatitis and are not to be missed, such as dermatomyositis. The broader differential diagnosis includes other connective tissue diseases (discoid lupus erythematosus [Figure 1], Sjögren’s, etc), psoriasis, contact urticaria, infections (viral, bacterial or fungal), and drug reactions. Neoplasms benign or malignant can also mimic dermatitis and can localize to an eyelid. Discussion of those conditions is beyond the scope of this chapter.

Figure 1.

Discoid lupus erythematosus plaques on the eyelids. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.


Contact dermatitis is comprised of allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD); these can be difficult to differentiate and have overlapping characteristics.

What to be alert for in the history

A careful history of exposures is critical to the diagnosis of contact dermatitis. These historical reviews can be quite extensive and occasionally require a referral to a contact dermatitis specialist within dermatology for a comprehensive workup. A flare in previously well controlled atopic or seborrheic dermatitis may represent a new allergic contact dermatitis and should prompt re-evaluation of exposures. It is high yield to ask the patient about occupation, hobbies, home and yard care responsibilities, and of course, cosmetics, skin care products, and prescription medications.

Irritant contact dermatitis (ICD) often presents with a history of burning or stinging skin, usually within minutes of application of offending product. Pruritus is more common with an allergic contact dermatitis (ACD), and the rash onset is usually reported 1 to 2 days after exposure to an allergen. Exposures (and their associated allergens) that can cause eyelid dermatitis:

–Eyelash curlers (nickel, rubber additives; Figure 2, Figure 3, Figure 4), chemicals contained in facial tissues (preservatives), make-up applicators (rubber additives), nail polish (tosylamide formaldehyde resin; Figure 5), artificial nails (acrylates; Figure 6), household cleaners (irritant reaction), ophthalmic solutions (preservatives, antibiotics, topical beta-blockers; Figure 7), shampoos (cocomidopropyl betaine; Figure 8, Figure 9), hair dye (paraphenylenediamine) and poison ivy/oak (urushiol).

Figure 2.

Eyelid dermatitis to eyelash curler. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

Figure 3.

Patch test positive to rubber portion of the eyelash curler. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

Figure 4.

Patch test positive to thiuram, rubber additive, also present in rubber. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs. portion of eyelash curler

Figure 5.

Allergic contact dermatitis to nail polish. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

Figure 6.

Allergic contact dermatitis to acrylic nails. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

Figure 7.

Irritant eyelid dermatitis to eyedrops. Erythematous scaly plaques present at the outer upper and especially outer lower eyelids, consistent with where the eyedrops would leak out of the eye. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

Figure 8.

Patch positive to shampoo ingredient, cocomidopropyl betaine Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

Figure 9.

Eyelid dermatitis–ACD to shampoo ingredient. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

–Facial or hand moisturizers (preservatives, formaldehyde releasers, sunscreen chemicals, lanolin)

–Various cosmetics including eyeliners, mascara, eyeshadow, lipstick (fragrances, formaldehyde releasers, shellac, sunscreen chemicals). Mascara causes an irritant reaction more often than allergic.

–Although nickel is not a common ingredient in cosmetic products, it has been hypothesized to contaminate products during manufacturing.

–Jewelry, keys, coins (nickel and gold) can transfer to skin from the handling of those metal objects by hands.

–Topical antibiotics (neomycin and bacitracin) are common over-the-counter self-remedies, which patients apply to inflamed skin in an attempt to treat it. Both are frequent causes of allergic contact dermatitis.

–Airborne allergens (urushiol, fragrances, lichens, other various botanicals)

Characteristic findings on physical examination

As eyelid dermatitis can be an episodic occurrence, patients can present with relatively normal eyelid examination. In general, eyelid dermatitis appears as erythematous, often scaly, sometimes crusty and oozing plaques on either upper or lower eyelids or both, unilateral or bilateral. Edema is often present, but not without erythema and scaling.

The palpebral and bulbar conjunctiva are usually spared, but can appear slightly erythematous as a reaction to the surrounding inflammation. Upper lid involvement is more associated with airborne contact allergens, whereas lower lid dermatitis is more commonly associated with contact dermatitis induced by eye drops. In a photodistributed dermatitis again lower eyelids will be involved, while upper eyelids, especially creases, will be spared.

Allergic or irritant dermatitis more often presents as acute eyelid dermatitis with intense pruritus, weeping, brightly erythematous and edematous papules and plaques. Although vesicles are also a hallmark of acute contact dermatitis, they are less common periorbitally. Presence of vesicles should alert the clinician to consider a herpetic viral infection (herpes simplex or zoster; Figure 10). Yellow honey-color crusting can also indicate bacterial impetiginization.

Figure 10.

Eczema herpeticum with punched out crusty papules and vesicles around the eyelids. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

Contact dermatitis is often bilateral. Unilateral involvement suggests an infectious cause such as herpes zoster or erysipelas. Hordeolum and chalazion usually localize to one eye as well.

If eyelids present with swelling (edema) in the absence of erythema, scaling or pruritus, other eyelid conditions need to be considered, such as angioedema or hypothyroidism-induced periorbital edema.

Expected results of diagnostic studies

Contact eyelid dermatitis is a clinical diagnosis in most cases, as history in combination with improvement when avoiding the allergen/irritant are enough to finalize diagnosis.

In more difficult cases, patch testing to a number of contact allergens can help distinguish a specific cause. Patch testing is the gold standard for evaluation of ACD. Unfortunately a large number of allergens thought to cause ACD of the eyelids are not found on the only patch test material approved by the Food and Drug Administration, the TRUE test, necessitating more extensive testing. Even once a relevant allergen has been identified, it can remain a challenge to eliminate contact with the substance or substances that cross-react with the allergen. For example “unscented” or “fragrance-free” formulations do not assure the elimination of fragrance cross-reactors.

Useful databases have emerged that can help identify products free of a patient’s known allergen. The Contact Allergen Management Program (CAMP) is maintained by and accessible to clinician members of the American Contact Dermatitis Society.

When vesicles are present, the preparation of a Tzanck smear or a viral culture can help rule out a herpes outbreak. Bacterial culture helps to identify a cause of impetigo.

Contact dermatitis is not usually examined by biopsy and separating allergic from irritant contact dermatitis is impossible by histology. The histology of both shows spongiotic dermatitis (intercellular edema) in early and subacute stages, sometimes with intra-epidermal eosinophils, and the thickened epidermis and papillary dermal fibrosis of lichen simplex chronicus with prolonged involvement.


What to be alert for in the history

Patients presenting with eyelid dermatitis caused by atopic dermatitis (AD) often have a history of chronic eyelid itching, redness and scaling; plus they often have eczema diagnosis since early childhood. Pruritus, sometimes unbearable, is often their main concern, as they become trapped in endless itch-scratch-itch cycles. Personal or family history of atopy (AD, or allergic rhinitis/hayfever or asthma) is typically present. AD is diagnosed on the basis of major criteria (family history of eczema, severe pruritus, facial and extensor distribution in infants, flexural distribution in adults) and numerous minor criteria. As nipple dermatitis is fairly specific for AD, asking about that symptom can confirm diagnosis.

Characteristic findings on physical examination

Atopic dermatitis is the most common cause of chronic eyelid dermatitis, which mimics changes seen in other chronic eczemas, with hyperpigmentation, lichenification, and diffuse scaling. Excessive chronic rubbing of the eyelids can cause eyelash and eyebrow hair loss. Dennie Morgan infraorbital folds, periorbital darkening (the “allergic shiner”), keratoconus, and anterior subcapsular cataracts are other clinical findings seen in chronic atopic eyelid dermatitis.

Full skin examination is important and helpful in identifying other typical areas of involvement by atopic dermatitis (Figure 11, Figure 12).

Figure 11.

Atopic dermatitis of eyelids. Chronic lichenified plaques with eyelid thickening and hair loss. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

Figure 12.

Chronic atopic dermatitis of eyelids. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

Expected results of diagnostic studies

Again, atopic dermatitis (AD) of eyelids is a clinical diagnosis, rarely requiring any diagnostic studies. As discussed with allergic and irritant contact dermatitis, swab cultures are sometimes necessary to evaluate for presence of a bacterial and/or viral infection that can complicate diagnosis.

Skin biopsy shows similar changes to contact and seborrheic dermatitis with acute or subacute spongiotic dermatitis early on, and psoriasiform spongiotic dermatitis or lichen simplex chronicus at later chronic stages. Laboratory testing of total serum IgE can be elevated (but not diagnostic), and skin prick tests for type I sensitizations are frequently positive (food allergies, pollens, dust mites), but again are not diagnostic of AD.


What to be alert for in the history

Patients with eyelid dermatitis due to seborrhea report scaling as their main concern; where as level of pruritus is usually variable. In addition to eyelid involvement, most complain of redness and scaling in several other sebaceous-rich areas of skin, such as the scalp, eyebrows, retroauricular skin, nasolabial creases, central chest, axilla, groin, and inframammary folds. Symptoms are often chronic with periods of exacerbation.

Characteristic findings on physical examination

Clinically, upper and lower eyelids demonstrate poorly circumscribed erythematous thin plaques with greasy yellow or fine white scale. When eyelash margin alone is affected and no other cutaneous findings are identified, seborrheic dermatitis of the eyelids is the most likely diagnosis (Figure 13). Skin examination of sebaceous-rich areas of the skin and their involvement by seborrheic dermatitis also helps to support the diagnosis.

Figure 13.

Seborrheic eyelid dermatitis as evident by yellow greasy scaly plaques that extend into the eyebrows, nasolabial folds, and forehead. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

Expected results of diagnostic studies

Seborrheic dermatitis is a clinical diagnosis. Rarely, tinea faciei can present with similar findings (Figure 14), and KOH examination can be helpful to rule out this fungal infection. If seborheic dermatitis, including seborrhea of the eyelids, is very severe or acute in onset, an HIV test should be ordered. The histology of seborrheic dermatitis depends on the age of the lesion biopsied, showing acute, subacute, or chronic/psoriasiform spongiotic dermatitis.

Figure 14.

Tinea faceii presented as scaly annular plaque on the lower eyelid. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.


What to be alert for in the history

Rosacea is a chronic inflammatory disorder mostly affecting fair skin individuals. Patients are usually adult females in a 30- to 60-year-old age group. Typical facial rosacea presents with facial flushing (triggered by stress, spicy food, heat, or alcohol), redness, and acne-like lesions. Symptoms are nonspecific and encompass stinging, burning and itching of the areas involved. Many report skin sensitivity to a variety of topical products and sun.

Topical and intranasal steroids are a common trigger of a persistent rosacea flare. Ocular rosacea can be present in the absence of the characteristic rosacea features. Variety of ocular and eyelid symptoms are reported: dry eyes, sensation of grittiness or foreign body, light-sensitivity and swelling, itching or scaling of the eyelids.

Characteristic findings on physical examination

Clinically, upper and lower eyelids can be erythematous, scaly and edematous, usually involving eyelash margin with greasy scaling. Mild to severe conjunctival injection can be present. Chronic inflammation can lead to lid thickening.

The most helpful findings are clinical signs of facial rosacea. Diffuse erythema and prominent telangiectasias on the cheeks, forehead, nose, and chin. Inflammatory papules and small pustules without comedones are seen in acneiform rosacea in the same distribution. Sebaceous hyperplasia and tissue hypertrophy can be seen over the central forehead, nose (rhinophyma) or chin predominantly in male patients. If none of the cutaneous findings of rosacea are present, referring patient to an ophthalmologist is recommended to confirm diagnosis. Prompt diagnosis of ocular rosacea is important, as undiagnosed and untreated it carries the risk of corneal scarring.

Expected results of diagnostic studies

Ocular rosacea is also a clinical diagnosis, and biopsy is rarely needed.


Dermatomyositis (DM) is an idiopathic inflammatory myopathy with characteristic skin findings, which often precede development of proximal muscle weakness by weeks to months. This is a rare condition that can overlap with other autoimmune rheumatic diseases. DM carries a risk of systemic complications related to muscle weakness (respiratory failure, dysphagia, bowel dysmotility) and an increased relative risk of malignancy.

What to be alert for in the history

Thirty to sixty percent of patients with DM have periorbital skin findings of DM, the heliotrope rash (Figure 15). Although it is asymptomatic, signs of periorbital darkening, fine scaling and especially eyelid swelling can be the initial concerns that bring a patient into a physician’s office. Patients with those findings should be asked about new photosensitivity, fatigue, muscle weakness, examples being difficulty with rising from a chair or brushing hair.

Figure 15.

Heliotrope rash of juvenile dermatomyositis. Photographs are courtesy of Dr Alfons Krol, Dr Eric Simpson and Dr Fran Storrs.

Characteristic findings on physical examination

Heliotrope rash is a violaceous or lilac discoloration of the periorbital eyelid skin, sometimes accompanied by significant edema or scaling (Figure 14). Other cutaneous signs of DM are erythematous to violaceous papules and plaques over the metacarpalphalangeal joints, also known as Gottron’s papules; the “V” sign of the anterior neck and the “shawl sign” described as macular erythema and poikiloderma (telangiectasia, atrophy, hypo- and hyperpigmentation).

Expected results of diagnostic studies

Diagnostic workup should include anti-nuclear antibody (ANA) screen as well as myositis-specific antibodies, muscle enzyme levels (creatine phosphokinase, aldolase), electromyography, and muscle biopsy (triceps most sensitive) or MRI. The extent of workup for malignancy is debated but can be guided by family history, patient symptoms, general physical examination (including rectal, pelvic and breast), and all age-appropriate cancer screening. Skin biopsy can be helpful in demonstrating subtle vacuolar interface dermatitis on histology.

Who is at Risk for Developing this Disease?

Risk factors for developing eyelid dermatitis are related to its varying etiologies; however, female patients are reported to comprise 90% of cases of eyelid dermatitis.

ACD is the most common cause of eyelid dermatitis, ranging from 50% to 76% of cases. ICD is sometimes counted together with ACD, hence it is difficult to estimate its prevalence.

Patients with a history of a primary dermatologic condition, such as AD, seborrhea, rosacea, psoriasis, are also at higher risk of developing contact (allergic or irritant) eyelid dermatitis due to already present alteration of skin barrier.

What is the Cause of the Disease?
Pathophysiology of various causes of eyelid dermatitis


The unique anatomy of the eyelid makes it a susceptible site for inflammation. With thickness about a fourth that of other facial skin (about 0.5mm) there is facile penetration of allergens or irritants. Auto-inoculation from distant sites or even close personal contacts is possible, and airborne exposures must be considered.

In allergic contact dermatitis the inflammation is mediated by a delayed (type IV) hypersensitivity reaction that occurs after sensitization. Commonly prescribed antihistamines used for type I IgE-mediated hypersensitivity are useful only for their soporific effects in type IV reactions.

Irritant dermatitis is mediated by direct toxic effect of a chemical whose physical properties such as hydrophobicity influence ability to penetrate the stratum corneum and cause cellular damage. Pre-existing disruption of the skin’s barrier, as is common in disorders like atopic dermatitis, may enhance the penetration of these molecules. Thus individual skin condition alters the threshold at which a chemical becomes an irritant and efforts to maintain skin hydration and barrier become important.


Atopic dermatitis (AD) is a common and genetically predisposed skin condition with initial symptoms developing in infancy or childhood and varying clinical patterns at different stages of life. The eyelids are a commonly involved site in AD owing to the thin nature of the area being easily traumatized by scratching. The associated condition icthyosis vulgaris is caused by defective or absent fillagrin, a protein critical in maintaining a normal skin barrier. The loss of fillagrin results in a retention hyperkeratosis characterized by hyperlinear palms, keratosis pilaris (follicular rough bumps on the upper arms and thighs), and xerotic fine scales on the extensor surfaces.

It is thought that the disrupted skin barrier in AD leads to more facile penetration and presentation of allergens accounting for the increased frequency of allergies seen. These patients are prone to secondary bacterial, fungal, and viral infections, have higher rates of staphylococcal colonization, often requiring antibiotic or antiviral therapy. This predispostion to infection is partially due to the impaired barrier function of the skin, but is also due to altered innate immunity, seen by decrease of endogenous antimicrobial peptides in atopic skin.


The pathogenesis of seborrhea is debated but largely thought to be secondary to epidermal colonization by the lipophyilic and nonpathogenic yeasts of the Malassezia and Pityrosporum species. An altered immune response is thought to be involved as evidenced by the more severe presentations found in the HIV/AIDS population. Severe seborrheic dermatitis is also often present in patients with Parkinson’s disease (Figure 14).


Pathophysiology of rosacea is poorly understood. Multiple etiologies have been suggested, including environmental triggers, altered antimicrobial peptides melieu, presence of skin bacteria and possibly Demodex folliculorum connection. Vascular proliferation and dermal degeneration contribute to development of erythematotelangiectatic rosacea. For ocular rosacea, specifically meibomian gland dysfunction resulting in altered tear film and irritation, was proposed as a potential etiology.

Systemic Implications and Complications

Systemic complications associated with eyelid dermatitis are rare.


Systemic contact dermatitis may result from a systemic exposure (injection or oral, intranasal, intravenous administration) to a contact allergen (or one that cross-reacts) in a patient who is already sensitized. Agents that have been reported to cause systemic allergic contact dermatitis include ethylenediamine, various antibiotics, corticosteroids, fragrances (balsam of Peru), propylene glycol, sorbic acids, metals, cashews, and mangos. Those patients will have extensive body dermatitis, not just eyelids.

Clinical features include a widespread eczematous eruption favoring the buttock and flexural areas, which may be accompanied by generalized systemic complaints including fever, malaise, nausea, and headaches. The diagnosis can be made by detailed history and patch testing as described previously.


Atopic dermatitis is commonly associated with respiratory allergy, asthma, and less commonly food allergies. Patients with atopic dermatitis are more susceptible to bacterial (Staphylococcus aureus) and viral infections (molluscum contagiosum, warts and herpes virus) due to disrupted barrier function, defects in cellular immunity and decreased levels of antimicrobial peptides that are usually present in the skin. Viral and bacterial cultures, Tzanck smears, or viral polymerase chain reaction asays (PCRs) can help make the diagnosis.

If herpes virus infection is suspected and involves the periocular region, prompt evaluation by an ophthalmologist is warranted to check for corneal involvement (herpes keratitis), which can lead to blindness if left untreated.

Keratoconus (conical cornea) is associated with chronic atopic dermatitis, and many studies suggest that excessive eyelid rubbing is the most causative factor in AD patients that develop keratoconus. Cataracts (subcapsular) have been described both as a manifestation of atopic dermatitis and as a complication of corticosteroid treatment. Currently cataracts associated with atopic dermatitis and corticosteroid therapy are indistinguishable clinically. Ophthalmologic examination is recommended in patients with symptoms of decreased vision and severe chronic eyelid disease.


Severe seborrheic dermatitis may be asociated with neurologic conditions, such as Parkinson’s disease, epilepsy, and multiple sclerosis. Severe recalcitrant seborrheic dermatitis has also been observed in patients with human immunodeficiency virus (HIV), and may be the presenting sign prompting HIV-1/2 antibody screening.


Ocular complications of rosacea include blepharitis, conjunctivitis, meibomian impactions, hordeola, corneal neovascularization, corneal ulcerations and scarring. Symptoms of recurrent blushing is common in patients with vascular rosacea. Rarely, the lymphatic vessels can be involved and can lead to persistant woody induration fo the central face, termed solid facial edema. Low grade fever, myalgias, leukocytosis and elevated erythrocyte sedimentation rate (ESR) can be seen in association with rosacea fulminans.


In patients with dermatomyositis, associated systemic findings include progressive symmetric proximal muscle weakness. Rarely patients can develop cardiac myositis and interstitial lung disease. Muscle disease may present before, concurrently, or after cutaneous manifestations. In adult patients (usually >50 years of age), dermatomyositis may be the presenting manifestation of an underlying malignancy. Age appropriate or symptom-directed malignancy screening should occur every 6 months for 2 years after diagnosis.

Treatment Options

Table 1. Treatment options for eyelid dermatitis (T – topical, S – systemic)

Table 1.
  First Line treatment   Second Line treatment  
Severity of condition Mild Moderate-Severe Mild Moderate-Severe
Allergic/ irritant contact dermatitis Avoid allergen or irritant(T): low potency topical steroid twice a day up to 10 dayseg, hydrocortisone 2.5% ointment Avoid allergen or irritant(T): mid-potency steroid (eg, triamcinolone 0.1% ointment) twice a day up to 5 days, followed by topical calcineurin inhibitors (TCIs; tacrolimus 0.1% ointment or pimecrolimus 1% cream) twice a day until resolution of symptoms Avoid allergen or irritant(T): TCIs (tacrolimus 0.1% ointment or pimecrolimus 1% cream) twice a day until resolution of symptoms Avoid allergen or irritant(S): short course of corticosteroid (eg, prednisone 40 to 60mg orally daily for 1 to 3 weeks)
Atopic dermatitis (T): low-potency topical steroid twice a day up to 10 days (T): mid-potency steroid twice a day up to 5 days, followed by TCIs (tacrolimus 0.1% ointment or pimecrolimus 1% cream) twice a day until resolution of symptoms(S): sedating antihistamines (eg,: hydroxyzine 25 to 50mg every evening to treat pruritus (T): over-the-counter barrier creams or ointments as needed (eg, petrolatum) (T): TCIs (tacrolimus 0.1% ointment or pimecrolimus 1% cream) twice a day until resolution of symptoms
Seborrheic dermatitis (T): ketoconazole 2% cream twice a day until resolutionluke warm compresseswashing eyelashes with baby shampoo to work out the scales (T): low potency steroid twice a day up to 10 days (T): ketoconazole 1% to 2%, selenium sulfide 2.5%, or over-the-counter zinc pyrithione, or salicylic acid-containing shampoo diluted 1:10; wash the areas daily until resolution (T): TCIs (tacrolimus 0.1% ointment or pimecrolimus 1% cream) twice a day until resolution of symptoms
Rosacea-induced eyelid dermatitis luke warm compresses to improve blepharitisartificial tears to help with ocular irritation (S): tetracycline class antibiotics. eg, minocycline 100mg orally twice a day or doxycycline 100mg orally twice a day for 6 weeks, then taper or stop (T):metronidazole 0.75% to 1% cream, gel, lotion or sodium sulfacetamide 10% lotion , cleanser (T): very short course of low- potency steroids up to 5 to 7 dayseg, hydrocortisone 2.5% cream or desonide 0.05% lotion

Optimal Therapeutic Approach for this Disease


When contact dermatitis is suspected, undergoing patch testing with a screening tray as well as patient’s personal products is often crucial to pinpoint a causative allergen or an irritant. If patch testing is not possible, then open application use test with a suspected topical product can be helpful.

Complete avoidance of the relevant allergen or irritant is paramount. Patient education should be thorough and patients should receive a printed list of the names and synonyms of all positive allergens. Suggestions for possible alternative to the allergenic products should be provided.

Treatment of acute disease should include the use of low-potency topical steroids in an ointment base twice daily for up to 10 days. Alternatively for more severe disease, mid-potency topical steroid in an ointment base can be used twice a day for 3 to 5 days, followed by the use of TCIs until the rash resolves. Although TCIs have minimal systemic absorption, black box warnings should still be discussed. Not uncommonly TCIs can cause local side effects such as burning and stinging.

Use of these agents after several days of low- to mid-potency topical steroids (after much of the acute inflammation has resolved) can minimize the discomfort. In severe disease, a short course of oral corticosteroids may be necessary; however, this should be reserved for cases in which the allergen is known and the exposure was limited. Treatment with topical steroids should be used with caution, as the eyelids are very thin and are more prone to the adverse side effects such as atrophy, and in chronic use cases can lead to glaucoma and cataracts.


For acute flare-ups, aggressive treatment with medium strength topical steroids in an ointment base for 3 TO 5 days may be necessary, followed by use of TCIs until clear (or low-potency topical steroids for 5 to 7 more days). application of cool compresses for 20 to 30 minutes prior to application of the topical steroid can be beneficial. However, cool compresses should be used with caution as it may lead to excessive dryness or irritation from repeated wet-to-dry cycling.

For chronic or persistent disease, daily to twice daily use of TCIs may be necessary. For mild disease, low-potency topical steroids twice daily up to 10 days are effective.

For maintenance, ample moisturization to restore the skin barrier is crucial. Examples of such agents include plain 100% white petrolatum, or thick over-the-counter moisturizing creams (eg, Cetaphil, Eucerin, Aquaphor, Aveeno). Elimination of potential irritants is also important in disease control.

Oral antihistamines such as diphenhydramine or hydroxyzine or doxepin can be used at bedtime to help break the itch-scratch cycle during sleep. Patients should be warned about the sedative side effects of these medications.


A variety of treatment options exists. The mainstay of eyelid and facial disease treatment is ketoconazole 2% cream. Shampoos containing salicyclic acid, selenium sulfide, zinc pyrithione and ketoconazole are generally used to treat scalp disease. These agents can also be used to treat the eyelids but should be diluted 1:10 to minimize irritancy. A short course of a low-potency non-fluorinated topical steroid can also be used to treat acute flares, however, the relapse rate is high. TCIs can be useful in severe cases or in those who fail to respond to low-potency topical steroids or are intolerant of ketoconazole cream.


Oral tetracyclines are an effective treatment option for moderate-to-severe ocular rosacea. Treatment should start with a higher dosing regimen (doxycycline or minocycline 100 to 200mg daily or tetracycline 250mg QID or 500mg BID) for 6 weeks, then tapering off completely or to a lower-dose maintenance regimen. Potential side effects of this class of medications include but are not limited to gastrointestinal upset (nausea, vomiting, diarrhea), vaginal yeast infections, photosensitivity, and rarely hypersensitivity skin reactions. Low-dose doxycycline/minocycline (50mg daily) and extended release formulations of those medications can be used if higher doses can not be tolerated.

For milder disease, proper eyelid hygiene can help reduce symptoms. This includes warm compresses for 5 to 10 minutes, accompanied by gentle massage of the tarsal plate toward the lid margin. This serves to turn over stale and stagnant lipid secretions from the meiobian glands. Artificial tears can also be helpful for dry eyes. Also topical antibiotics applied to the lid margins can be helpful in decreasing the bacterial flora. Topical corticosteroids occasionally can be used to control severe flares, however, long-term use is discouraged, as it can lead to glaucoma and cataracts, as well as exacerbation of acneiform-type rosacea on the rest of the face.


Systemic treatment of dermatomyositis often depends on the level of muscle inflammation or symptoms of weakness, as well as severity of skin involvement. Such treatments are beyond the scope of this chapter.

Patient Management


Regardless of the etiologies of eyelid dermatitis, if the patient has severe enough disease to warrant oral steroids or mid-potency topical steroids, the patient should be seen back in clinic in 2 to 4 weeks.

In cases of mild-to-moderate disease in which low-potency topical steroids are being used, then follow-up visits are still encouraged but can be postponed to every 2 to 3 months.

Signs of steroid overuse (atrophy, telangiectasias, striae), cataracts (corneal opacities), symptoms of glaucoma and infections should be monitored at every visit. Patients with severe atopic eyelid dermatitis should be followed regularly by ophthalmology. The side effects of topical corticosteroids increase with the longer duration and higher potency steroids. TCIs should be used if disease can not be cleared with a 7 to 10 days course of topical corticosteroids.

Patients with ocular rosacea should be followed every 3 months if they are on an oral medicaton for their disease. They should also be advised to see an ophthalmologist for periodic evaluation. Women of child-bearing age on tetracyclines should be appropriately counseled to stop the medication if they are planning on becoming pregnant, as it can lead to dental anomalies in a fetus. In patients taking minocycline, blue-gray pigmentary changes are possible 12 to 24 months into treatment, hence an alternative medication plan is needed after patient has taken minocycline for more than 1 year.


For long- term maintenance therapy of severe disease, it is important to minimize the long-term use of higher potency topical steroids. For severe disease, patients should include daily or twice daily use of TCIs. Sometimes use of topical steroids is also needed for maintenance therapy, but should be limited to twice a week use in such cases. Using low-potency topical steroids on the weekends and moisturizers or TCIs during the rest of the week can be a reasonable maintenance plan.

For moderate disease twice a week use of low-potency topical steroids with barrier replacement therapy (moisturization) on the other days is safe and efficatious. For mild disease, barrier replacement therapy (moisturization with plain 100% petrolatum) is the mainstay. For diseases like atopic dermatitis, barrier replacement therapy is crucial to help patients stay in remission longer.

Unusual Clinical Scenarios to Consider in Patient Management

One particular conundrum that patients with eyelid dermatitis face is the development of an allergic contact dermatitis to the product that they are using to treat their condition. As alluded to earlier, a flare in previosly well controlled eyelid dermatitis or eyelid dermatitis that has suddenly became resistant to therapy should prompt evaluation for all topical contact exposures. Examples include ACD to topical steroids, topical antibiotics, preservatives, or inactive ingredients within medications. Use of petrolatum/ointment base preparations can help minimize such events, as even fragrances make their way into some topical steroid preparations. Repeat patch testing should be considered.

What is the Evidence?

Amin, KA, Belsito, DV. “The aetiology of eyelid dermatitis: a 10-year retrospective analysis”. Contact Dermatitis. vol. 55. 2006. pp. 280-5. (This retrospective study evaluated more than 1200 patch test patients, 8% of which had eyelid dermatitis. Allergic contact dermatitis was the most common cause, surpassed only by seborrheic dermatitis when the eyelids alone were affected.)

Goossens, A. “Contact allergic reactions on the eyes and eyelids”. Bull Soc Belge Ophthalmol. vol. 294. 2004. pp. 11-7. (This large study examined more than 1500 patients with conjunctivitis or eyelid dermatitis and found allergic contact dermatitis in 56% of patients tested. The study reviews classes of allergens, their sources, and modes of exposure.)

Guin, JD. “Eyelid dermatitis: experience in 203 cases”. J Am Acad Dermatol. vol. 47. 2002. pp. 755-65. (This article reviews 203 cases of eyelid dermatitis. With patch testing and ancillary tests a relevant allergic contact dermatitis was found in 76% of patients. Among the 12% of patients that had atopic dermatitis, 70% had a relevant allergen. Seborrheic dermatitis, psoriasis, and connective tissue disease each constituted less than 5% of cases.)

Papier, A, Tuttle, DJ, Mahar, TJ. “Differential diagnosis of the swollen red eyelid”. Am Fam Physician. vol. 76. 2007. pp. 1815-24. (A useful overview for general practitioners who are likely to see a mixture of primary dermatologic conditions as well as trauma, infection, and malignancy.)

Peralejo, B, Beltrani, V, Bielory, L. “Dermatologic and allergic conditions of the eyelid”. Immunol Allergy Clin North Am. vol. 28. 2008. pp. 137-68. (A broad literature review of eyelid dermatoses, their diagnosis, and treatment.)

Rietschel, RL, Warshaw, EM, Sasseville, D, Fowler, JF, DeLeo, VA, Belsito, DV. “North American Contact Dermatitis Group. Common contact allergens associated with eyelid dermatitis: data from the North American Contact Dermatitis Group 2003-2004 study period”. Dermatitis. vol. 18. 2007. pp. 7(Examining data on patients with exclusively eyelid dermatitis, patients screened by patch testing of 65 allergens had a relevant positive exposure 72% of the time. 65% of these positives could be attributed to a shorter list of only 26 allergens, a series proposed as a potential screening set for eyelid dermatitis.)

Zug, KA, Palay, DA, Rock, B. “Dermatologic diagnosis and treatment of itchy red eyelids”. Surv Ophthalmol. vol. 40. 1996. pp. 293-306. (Asuccinct review focusing on the physical examination, history, and differential diagnosis of the inflamed eyelid.)