Ocular Allergy
Allergies are thought to affect approximately 20% of the US and European populations; more than 50% of patients who seek treatment for allergies present with ocular symptoms. Allergic ocular disease is a common problem in children and is often associated with asthma, allergic rhinitis, and atopic dermatitis. Marked itching and bilateral conjunctival inflammation of a chronic, recurrent, and possibly seasonal nature are hallmarks of external ocular disease of allergic origin. Other signs and symptoms may be nonspecific and include tearing, stinging, burning, and photophobia.
Four specific types of ocular allergy are discussed in this section: seasonal and perennial allergic conjunctivitis, vernal keratoconjunctivitis (VKC), and atopic keratoconjunctivitis (AKC). All have some element of a type I hypersensitivity reaction caused by the interaction between an allergen and specific immunoglobulin E antibodies on the surface of mast cells in the conjunctiva. This interaction initiates a cascade of biochemical events involved in mediation of the allergic response. Among the mediators released is histamine, which causes much of the itching, vasodilation, and edema that are characteristic of the ocular allergic response.
Seasonal and perennial allergic conjunctivitis
Seasonal allergic conjunctivitis is a common clinical entity that affects approximately 40 million people in the United States, including many children. It occurs in the spring and fall and is triggered by environmental contact with specific airborne allergens such as pollens from grasses, flowers, weeds, and trees. Patients typically present with red and watery eyes, boggy-appearing conjunctiva, and ocular itching (Fig 20-9). Blue-gray to purple discoloration of the lower eyelids, termed allergic shiners, can occur secondary to venous stasis from nasal congestion.
The signs, symptoms, and presentation of perennial allergic conjunctivitis are similar to those of seasonal allergic conjunctivitis. Perennial allergic conjunctivitis is a type I hypersensitivity reaction that occurs after contact with ubiquitous household allergens, such as dust mites and dander from domestic pets. This condition is diagnosed based on the history and clinical presentation.
Treatment of all ocular allergy disorders is fundamentally similar to that of other allergy-related disorders. The most effective treatment is to avoid offending allergens or remove them from the patient’s environment. Unfortunately, avoidance may not be possible and complete removal may not be adequate to alleviate the patient’s symptoms. Medical treatment can be systemic or topical. Although oral antihistamines may be less effective at relieving specific ocular symptoms, they are often better tolerated in children, who may not accept eyedrops.
Topical medications include mast-cell stabilizers, H1-receptor antagonists, antihistamines, vasoconstrictors, corticosteroids, or combinations of these drugs (Table 20-2). H1-receptor antagonists can be used on an as-needed basis, but mast-cell stabilizers must be used for a few days before an effect is seen. In addition, mast-cell stabilizers should be used continuously through the allergy season to maximize their effectiveness. Nonsteroidal anti-inflammatory drops should be used with caution; cases of corneal perforation, though rare, have been reported. Topical corticosteroid drops used in pulsed doses can effectively reduce severe allergic ocular symptoms, but patients must be closely monitored for adverse effects, including glaucoma and cataracts.
Table 20-2 Topical Drops for Treatment of Allergic Ocular Disorders
Vernal keratoconjunctivitis
Vernal keratoconjunctivitis (VKC) is caused by type I and type IV hypersensitivity reactions. This condition most commonly affects males in the first 2 decades of life and, like seasonal allergic conjunctivitis, usually occurs in the spring and fall. There are 2 forms of VKC: palpebral and limbal (or bulbar). Both types manifest with severe itching. The limbal form is more common in patients of African or Asian descent and is more prevalent in warm, subtropical climates.
Clinically, the palpebral form of VKC preferentially affects the tarsal conjunctiva of the upper eyelid. In the early stages, the eye may be diffusely injected, with little discharge. There may be no progression beyond this stage. However, papillae may multiply, covering the tarsal area with a mosaic of flat papules (Fig 20-10). A thick, ropy, whitish discharge may be present.
The limbal form of VKC manifests early with thickening and opacification of the conjunctiva at the limbus, usually most marked at the upper margin of the cornea. The discrete limbal nodules that appear are gray, jelly-like, elevated lumps with vascular cores. A whitish center filled with eosinophils and epithelioid cells may appear in the raised lesion. This complex is called a Horner-Trantas dot. Limbal nodules may increase in number and become confluent (Fig 20-11). They persist as long as the seasonal exacerbation of the disease lasts.
The cornea may become involved, with punctate epithelial erosions, especially superiorly. Corneal involvement may progress to a large, confluent epithelial defect, typically in the upper half of the cornea, called a shield ulcer. The ulcer is sterile and clinically resembles an ovoid corneal abrasion (Fig 20-12).
Treatment of VKC is usually less effective than that of seasonal allergic conjunctivitis. Eyedrops combining a mast-cell stabilizer and an H1-receptor antagonist may be used initially. In addition, treatment of VKC often requires topical steroids or topical cyclosporine. Supratarsal injection of corticosteroids may be used in patients with refractory palpebral VKC.
Atopic keratoconjunctivitis
Atopic keratoconjunctivitis is a nonseasonal disorder that occurs in patients with atopic disease. It is relatively rare in children. See BCSC Section 8, External Disease and Cornea, for further discussion.
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.