Allergic Eye Diseases, Episcleritis and Scleritis

Published on 08/03/2015 by admin

Filed under Opthalmology

Last modified 08/03/2015

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5 Allergic Eye Diseases, Episcleritis and Scleritis


Allergic eye disease in its various forms is a common cause of ocular morbidity in both primary care and specialist practice. The external eye is under constant immunological challenge from a wide variety of substances; this may lead to the development of one of many conditions that can be loosely grouped as ‘allergic eye disease’. The chief factors determining the outcome of such challenges are the severity and duration of the antigenic load and the immunological status of the individual. Local or systemic immune mechanisms may be involved to produce immediate hypersensitivity, complement-mediated or delayed hypersensitivity reactions. The spectrum of allergic conjunctivitis (Table 5.1) ranges from mild self-limiting seasonal conjunctivitis to atopic keratoconjunctivis in which vision is threatened by corneal vascularization, herpetic epithelial infection and the long-term complications of topical corticosteroid therapy. Although patients complain of red, sore and discharging eyes, itchiness is the characteristic symptom of allergic eye disease. Patients also have an increased risk of keratoconus and atopic cataract. Increased levels of IgE and eosinophils are found in the conjunctiva and a wide range of inflammatory mediators have been shown to be involved in the pathogenesis.

Treatment involves identification and avoidance of the offending antigen and the administration of antihistamines, mast cell stabilizers or steroids. Mild disease responds to topical antihistamine or mast cell-stabilizing agents alone but corneal involvement requires topical steroids, often over prolonged periods with surveillance for steroid side-effects.



Vernal keratoconjunctivitis (VKC) is an ocular manifestation of atopy. There is frequently a history of eczema, hayfever and asthma which characteristically starts early in life. The disease is bilateral and chronic with seasonal exacerbations and remissions and predominates in young males. It is common in the hot dry climate of the Middle East. Patients are usually allergic to multiple antigens and have seasonal exacerbations, often improving around puberty. Itching and ocular discomfort with mucoid discharge are the predominant symptoms.

The aim of treatment during acute exacerbations is to control symptoms by reducing conjunctival inflammation. In less severe forms of the disease single agents may be successful in controlling the disease but in severe cases intensive topical steroids are usually needed. Mucolytic preparations such as acetylcysteine drops can be useful in removing excess mucus. It is important to reduce topical steroids as soon as possible to avoid ocular complications such as glaucoma and this may be facilitated by the additional use of a mast cell-stabilizing drop for its steroid-sparing effect.


This is a heterogenous group of conditions in which the skin, eye and mucous membranes are damaged through immune reactions giving rise to, amongst other effects, a cicatrizing conjunctivitis. Included in this group are cicatricial pemphigoid, erythema multiforme or Stevens–Johnson syndrome, linear IgA disease, dermatitis herpetiformis and some drug-induced disorders. The diagnosis, which involves the cooperation of ophthalmologist and dermatologist, may depend on tissue biopsy and immunohistochemistry. Bulbar conjunctival biopsies can be taken without risking disease exacerbation and biopsy of skin or other mucosal lesions may also be useful to support a diagnosis.


This autoimmune disorder is caused by autoantibodies to mucosal basement membrane. About 70 per cent of patients presenting with cutaneous pemphigoid have ocular changes, whereas in those presenting with ocular disease about 20 per cent have cutaneous disease. The condition usually presents to the ophthalmologist in elderly women as bilateral chronic conjunctival inflammation; the presentation is acute in a minority, and in some follows conjunctival or lid surgery. The clinical diagnosis of pemphigoid is suggested by the presence of one or more of the other features of the disease, which include scalp lesions and oesophageal, buccal and genital ulceration. Not all features may be present, nor are they necessarily all active simultaneously, but it may be possible to find scarring as evidence of earlier activity.

The clinical course is of progressive conjunctival shrinkage with acute inflammatory exacerbations. Patients need to be assessed for the degree of conjunctival fibrosis and the amount of active inflammation. In the early stages there is symblepharon formation in the lower fornix, with loss of the caruncle. With active disease, areas of conjunctival ulceration stain with fluorescein and resolve with further scarring. Progressive conjunctival scarring leads to increasing symblepharon formation, entropion and tear film instability, which in turn causes corneal opacification. In mild, slowly progressive disease, therapy may not be justified. First-line treatment is with dapsone or sulfapyridine, but severe progressive disease may require more potent systemic immunosuppressive drugs.