PATHOGENESIS

One or more manifestations of atopic keratoconjunctivitis (AKC) develop in approximately one-third of patients with atopic dermatitis. Atopic individuals show signs of type I hypersensitivity responses as well as depressed systemic cell-mediated immunity. As a consequence of this altered immunity, they are susceptible to herpes simplex virus keratitis and colonization of the eyelids with Staphylococcus aureus. Complications related to this predisposition to infection may contribute to, or compound, the primary immunopathogenic manifestations. AKC is primarily a type IV reaction; therefore, the use of mast-cell therapy may not be effective.

CLINICAL PRESENTATION

The ocular findings of AKC are similar to those of VKC (discussed earlier in the chapter), with the following differences:

• Patients with AKC frequently have disease year-round, with minimal seasonal exacerbation.

• Patients with AKC are older.

• The papillae are more apt to be small or medium-sized than giant.

• The papillae occur in the upper and lower palpebral conjunctiva.

• Milky conjunctival edema, with variable subepithelial fibrosis, is often present (Fig 11-6).

• Extensive corneal vascularization and opacification secondary to chronic epithelial disease (likely due to some degree of direct trauma from eyelid changes and/or limbal stem cell dysfunction) can occur (Fig 11-7).

• Eosinophils in conjunctival cytology specimens are less numerous and are less often degranulated.

• Conjunctival scarring often occurs, with occasional symblepharon formation.

• Posterior subcapsular and/or multifaceted or shield-shaped anterior subcapsular lens opacities may develop.

• Corneal findings include persistent epithelial defects, an increased incidence of ectatic corneal diseases such as keratoconus and pellucid marginal degeneration (possible association with eye rubbing), and an increased incidence of staphylococcal and herpes simplex infections.

Figure 11-6 Atopic keratoconjunctivitis demonstrating small papillae, edema, and subepithelial fibrosis.

Figure 11-7 Severe corneal vascularization and scarring with atopic keratoconjunctivitis.

MANAGEMENT

Treatment of AKC involves allergen avoidance and the use of pharmacotherapeutic agents similar to those used in the treatment of VKC. Cold compresses may also be of benefit. In addition, patients should be carefully monitored for complications of infectious diseases that may warrant specific therapy, such as secondary staphylococcal infections and herpes simplex keratitis, which is more common and more likely to be bilateral in patients with AKC (see Chapter 9).

In severe cases, the indications for systemic therapy include chronic ocular surface inflammation unresponsive to topical treatment, ocular discomfort, progressive cicatrization, and peripheral ulcerative keratopathy. Systemic immunosuppression (eg, cyclosporine or tacrolimus) should be monitored in coordination with an internist or rheumatologist. Systemic treatment of AKC may be beneficial in suppressing the interleukin-2 (IL)-2 response, which promotes lymphocyte proliferation.

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García DP, Alperte JI, Cristóbal JA, et al. Topical tacrolimus ointment for treatment of intractable atopic keratoconjunctivitis: a case report and review of the literature. Cornea. 2011; 30(4):462–465.

Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.