Signs and Symptoms

Contact dermatitis is an inflammatory reaction of the skin, including the eyelid(s) and periocular adnexa. The presentation may occur unilaterally or bilaterally, depending upon the antigenic exposure. In acute cases, the patient may present with diffuse lid erythema and edema, as well as pruritic vesicles or bullae.1 Chronic cases may show eczema, a characteristic thickening and scaling of the involved skin typically seen in atopic dermatitis.2

Common symptoms in both the acute and chronic forms of contact dermatitis include intense itching and burning of the skin and eyes, and associated tearing. The conjunctiva may also be involved, demonstrating variable bulbar injection and chemosis when included. Palpebral follicles may be seen in severe cases. Corneal involvement is rare, though chronic eye rubbing may lead to punctate keratopathy or epithelial erosion. Vision is not typically affected to any substantial degree, and preauricular lymphadenopathy is characteristically absent.

The history is of paramount importance in correctly diagnosing contact dermatitis. Many cosmetics, cleaning agents, fabrics, fragrances, medications, nickel and even metallic jewelry can be implicated in this skin reaction.2-4 Typically, since the reaction connotes some acute exposure to an offending allergen, it is assumed that the patient recently encountered something “new.” However, many agents implicated in contact dermatitis represent weak sensitizers, and the exposure may occur over weeks, months or even years.4 In cases involving the ocular tissues, one should give particular consideration to those substances which are readily applied or coincidently touch the skin around the eyes—particularly makeup (eyeliner, eye shadow, mascara) or makeup remover, sunscreen, contact lens solutions or metal spectacle frames. A wide range of ophthalmic medications may also have the capacity to induce allergic contact dermatitis.5


Contact dermatitis may be subdivided into several categories: irritant contact dermatitis, allergic contact dermatitis and photoallergic contact dermatitis.

Irritant contact dermatitis (ICD) accounts for nearly 80% of all cases of contact dermatitis seen clinically.1 The condition, also referred to as non-allergic contact dermatitis, represents a non-preprogrammed, non-immunologic, local inflammatory reaction to a chemical or physical irritant. This may include substances such as soaps or detergents, solvents (e.g., paint thinner, acetone) or particulate matter such as fiberglass insulation. Typically, the severity of the ICD reaction is proportionate to the amount and duration of irritant exposure. The mechanism of action involves a direct, local cytotoxic effect on the epidermis, leading to subsequent keratinocyte damage.6

The most important detail to recognize about ICD is that it can affect any individual, regardless of their immune status. A well-known example of ICD involves exposure to the plant Toxicodendron radicans, better known as poison ivy. Atopic individuals are especially susceptible to ICD, and may have a lower threshold for irritant exposure.

Allergic contact dermatitis (ACD), by its very definition, affects only individuals who are genetically preprogrammed toward allergic hypersensitivity. Like all allergic reactions, ACD occurs in two phases: a sensitization process, in which specific antibodies are generated toward the allergen, and an elicitation phase, in which the actual cellular response occurs. The mechanism of ACD involves a delayed, or Type IV, hypersensitivity reaction.6 This is a cell-mediated response, which employs discrete subpopulations of T-lymphocytes and immunoregulatory cytokines, including tumor necrosis factor alpha and interleukins 1, 13 and 18.7 Mast cells, which play a pivotal role in immediate Type I hypersensitivity reactions such as allergic conjunctivitis, are not central to Type IV reactions like ACD. However, the mast cell still has an important function, as it indirectly helps to control neutrophil recruitment.8

Photoallergic contact dermatitis (PACD) is an eczematous skin reaction initiated by an otherwise benign substance on the skin that becomes noxious when exposed to ultraviolet light. We refer to substances that induce PACD as photosensitizing agents. PACD characteristically occurs only with areas of exposed skin, such as the hands and face. Known photosensitizing agents include tar-based products, octyl dimethyl PABA (an ingredient in some commercial sunscreen formulas), certain forms of vegetation (including carrot, lemon and mustard plants) some oral antibiotics, such as tetracycline, and topical NSAID medications, such as ketoprofen, diclofenac and indomethacin.9,10


In cases of contact dermatitis, attempts should be made to identify the causative agent. Often, this can be accomplished with a careful history, but in more challenging cases epicutaneous patch testing can help to isolate the offending substance. Patch testing involves standardized samples of known allergens, placed on small delivery vehicles and applied to the skin of the upper back for two days.11,12 The test is typically performed only by an experienced dermatologist.

Once identified, the ideal long-term solution is to remove or avoid the causative agent. Short-term management involves emollients, treatment of secondary infection (if present) and downregulation of the immune response. The easiest method of arresting and reversing the outspilling of chemical modulators is the cold compress. Here, vasoconstriction slows the spread of edema and begins to limit the reaction.

Topical corticosteroids are the first-line medicinal therapy for most individuals, since these agents directly suppress the recruitment of polymorphonuclear leucocytes and reverse capillary permeability.12 Low-potency steroids such as hydrocortisone and desonide may be safer for use on the face, though stronger steroids such as clobetasol proprionate (Olux, Stiefel Labs) or betamethasone dipropionate (Diprolene, Merck) can be employed for moderate to severe disease.13 Steroid creams or lotions (preferable to ointments) used twice daily for 10-14 days are usually very effective. Care must be taken to apply these preparations only to the skin of the lids and ocular adnexa, as they are not appropriate for use in the eye.

Stronger periocular steroids may precipitate intraocular pressure elevation and should be monitored carefully. Also, it is important to note that topical steroids may in some cases themselves be allergenic, confounding the management of these patients.14 Calcineurin inhibitors such as tacrolimus (Protopic ointment, Astellas) and pimecrolimus (Elidel cream, Medicis) may benefit subjects who are poor candidates for topical corticosteroid therapy.12 More severe cases may require systemic corticosteroids. Oral prednisone (0.5-1mg/kg/d for 2-3 days, and tapered over 1-2 weeks) is the preferred course of therapy for recalcitrant contact dermatitis.1,6

The use of antihistamines is somewhat controversial in managing contact dermatitis. Since histamine release from mast cells is not central to the pathophysiology of the disorder, antihistamines would seem to be superfluous. However, oral agents such as cetirizine 10mg (Zyrtec, McNeil) or desloratadine 5mg (Clarinex, Merck) once daily may help to curtail the itching to some extent, and hence may be beneficial in addition to topical corticosteroid therapy.

For conjunctivitis associated with contact dermatitis, supportive therapy is beneficial. This includes, first and foremost, cold compresses and liberal use of ocular lubricants. Topical antihistamine/mast cell stabilizer products (e.g., Pataday, Alcon; Lastacaft, Allergan) once daily may provide palliative relief of conjunctival itching, as well as ocular swelling and hyperemia. More severe involvement, however, may warrant topical ophthalmic corticosteroids, such as prednisolone acetate 1% (Pred Forte, Allergan) or loteprednol etabonate 0.5% (Lotemax, Bausch + Lomb) every 2-4 hours for several days.

Clinical Pearls

The skin of the eyelid, by virtue of its anatomically thin structure, is particularly susceptible to inflammation by irritant or allergic contact dermatitis. Profound reactions may be seen in this area.

The differential diagnosis of contact dermatitis must include more extreme conditions such as preseptal cellulitis, orbital cellulitis, chlamydial infection, oculoglandular conjunctivitis and carotid cavernous fistula. A vesicular or pustular presentation warrants investigation for herpes zoster or simplex blepharitis.

Contact dermatitis is self-limiting only in cases where the inciting agent is identified and removed. Therapy with anti-inflammatory agents and palliative anti-allergy products can hasten the recovery and provide significant amelioration of symptoms.

Patients should be counseled that topical and oral steroids can raise intraocular pressure as well as thin the skin. Anyone placed on these agents must be reassessed to rule out these complications.

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8. Biedermann T, Kneilling M, Mailhammer R, et al. Mast cells control neutrophil recruitment during T cell-mediated delayed-type hypersensitivity reactions through tumor necrosis factor and macrophage inflammatory protein 2. J Exp Med. 2000 Nov 20;192(10):1441-52.

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11. White JM. Patch testing: what allergists should know. Clin Exp Allergy. 2012 Feb;42(2):180-5.

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14. Gonul M, Gul U. Detection of contact hypersensitivity to corticosteroids in allergic contact dermatitis patients who do not respond to topical corticosteroids. Contact Dermatitis. 2005 Aug;53(2):67-70.