Acute Allergic Conjunctivitis: Seasonal/Perennial
Acute allergic conjunctivitis is a type I immediate hypersensitivity reaction mediated by immunoglobulin E (IgE) and subsequent mast-cell activation, stimulated by direct exposure to environmental allergens. The reaction may be limited to the eye, or it may be part of a generalized allergic reaction with nasal and respiratory symptoms. Often a family history of atopy is present. Cytological examination of conjunctival scrapings shows eosinophilic infiltration. Elevated levels of IgE and histamine are found in the tear film. Acute allergic conjunctivitis is divided into seasonal allergic conjunctivitis (SAC) and perennial allergic conjunctivitis (PAC). The onset of symptoms for SAC is seasonally related to circulating aeroantigens. PAC is considered a variant of SAC that persists throughout the year, although seasonal exacerbations often are seen. Clinical symptoms and signs are typically bilateral and consist of itching, burning, and mild to moderate injection that can progress to various degrees of chemosis with superior tarsal conjunctiva papillary reaction. A watery or mucoid “stringy” discharge may be seen.
Chronic Atopic Keratoconjunctivitis
Chronic atopic keratoconjunctivitis (AKC) is an inflammatory disease that can lead to disabling symptoms involving both the conjunctiva and the cornea. It can present between the late teens through the fifth decade and has a slight male predilection. A large majority of patients have concomitant eczema or asthma. Between 20% and 40% of patients with atopic dermatitis also have AKC. Clinical symptoms include intense bilateral itching, tearing, burning, photophobia, blurred vision, and a stringy mucus discharge. Periorbital eczema, lid edema, conjunctival chemosis, and allergic shiners are common findings. Papillary hypertrophy of the upper tarsal conjunctiva is the most common sign ( Fig. 4.7.1 ). Cobblestone papillae on the superior tarsal conjunctiva also may occur. Gelatinous limbal hyperplasia and nodules may be present with or without Horner–Trantas dots (areas of eosinophils and degenerating cellular debris). In severe cases, cicatrizing conjunctivitis with subepithelial fibrosis, symblepharon formation, and forniceal shortening may develop. Histopathologically, a mixture of mast cells, eosinophils, and lymphocytes are found in the conjunctival epithelium.
Vernal Conjunctivitis
Vernal conjunctivitis is a bilateral, recurrent inflammation of the conjunctiva that tends to occur in children and young adults with a history of atopy. Its onset is most common in the spring and summer months, and the inflammation often goes into remission during the cooler months. The highest incidence is in the warm, temperate Middle East–Mediterranean region and Mexico. Boys are affected twice as often as girls, with a peak incidence between ages 11 and 13 years. Recent studies have found an association between low serum vitamin D levels in children with vernal conjunctivitis. The prominent symptom is intense pruritus. Other complaints include photophobia, burning, tearing, mild ptosis, and a thick, ropy, yellow, mucoid discharge. It is classically thought to be an IgE-mediated type 1 hypersensitivity reaction; however, studies have also noted T helper 2 lymphocyte involvement in a type IV immune reaction.
The three forms of the vernal conjunctivitis are palpebral, limbal, and mixed. The palpebral form is marked by cobblestone papillae on the superior tarsal conjunctiva ( Fig. 4.7.2 ) with minimal involvement of the lower lid. After initial papillary hypertrophy, the connective tissue of the substantia propria undergoes hyperplasia and proliferation to form giant papillae. The pressure of the cornea flattens the tops of the giant papillae to produce a cobblestone pattern. Tiny twigs of vessels are found in the centers of the papillae, which help differentiate these from the large follicles without the central vessels seen in trachoma. The limbal form is marked by a broad, thickened, gelatinous opacification of the superior limbus that can override the cornea ( Fig. 4.7.3 ). Tiny, twig-like vessels arise in the centers of these rounded lumps, as opposed to limbal follicles, where the vessels appear around the sides of the elevations. Histologically, the tissue is infiltrated with lymphocytes, plasma cells, macrophages, basophils, many eosinophils, and an increased number of conjunctival goblet cells ( Fig. 4.7.4 ). Horner–Trantas dots, which are white, chalk-like gelatinous nodules composed of eosinophils and epithelial debris located at the limbus, are characteristic in limbal vernal keratoconjunctivitis (VKC). Patients with VKC also have elevated levels of histamine with other cytokines and immunological molecules in the tear film.
The cornea is involved in about half the cases. Corneal manifestations include a superficial pannus and a punctate epithelial keratitis. Small, gray patches of necrotizing epithelium may involve the upper one third to two thirds of the cornea—in severe cases, the cornea appears to be dusted with flour. The affected area stains with fluorescein. A vernal “shield ulcer” develops as a horizontal oval, shallow, nonvascularized, indolent ulcer of the superior cornea (see Fig. 4.7.4 ) that leads to severe discomfort. The edges are composed of shaggy, gray, dead epithelial cells, and infiltration of the underlying superficial stroma is present. After the ulcer heals, a mild corneal opacity may persist at the level of Bowman’s layer.
Treatment of Allergic/Atopic Keratoconjunctivitis
Treatment of all of the above conditions is based on the severity and chronicity of the disease in each patient. For all cases, cold compresses, preservative-free artificial tears (refrigerated), and avoidance of allergens can help alleviate symptoms. Unfortunately, avoidance of the offending antigens is often difficult, thus medications are used for further symptomatic control ( Table 4.7.1 ).
| Category | Examples | Comments |
|---|---|---|
| Histamine 1 (H 1 ) receptor agonists | Levocabastine, emedastine difumarate | Use for isolated, acute allergic attacks. Use alone or in combination with mast-cell stabilizers and nonsteroidal anti-inflammatory drugs (NSAIDs). |
| Mast-cell stabilizers | Cromolyn sodium, lodoxamide, pemirolast, nedocromil sodium | Most useful for chronic allergies. May take 1–2 weeks to be effective. Pemirolast and nedocromil have antihistamine effects as well. Nedocromil also reduces eosinophil and neutrophil chemotaxis. |
| Antihistamines with mast cell–stabilizing activity | Olopatadine, alcaftadine, bepotastine, ketotifen fumarate, azelastine, epinastine, bepotastine | These medications combine the immediate effect of selective antihistamines with the long-term effects of mast-cell stabilization. They have convenient once- or twice-a-day dosing. Ketotifen and azelastine have anti-inflammatory properties as well. |
| Topical NSAIDs | Ketorolac, nepafenac, bromfenac | Can reduce itching, but stings when applied. |
| Vasoconstrictors | Naphazoline/pheniramine, naphazoline/antazoline | Available over the counter; instruction must be given to avoid chronic use because of the risk of rebound redness; relieves redness, but not other symptoms. |
| Topical corticosteroids | Loteprednol, fluorometholone, rimexolone | May be useful in serious cases or until control is achieved with other agents. Side-effects limit chronic use. |
| Oral antihistamines | Fexofenadine, loratadine, cetirizine, ebastine, mizolastine, desloratadine | Useful when systemic allergic symptoms are present but may cause dry eyes. |
| Immunomodulators | Tacrolimus, cyclosporine | Useful in refractory cases or situations where corticosteroid use is not appropriate. |
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