VERNAL KERATOCONJUNCTIVITIS (VKC) OR SPRING CATARRH It is a recurrent, bilateral, interstitial, self-limiting, allergic inflammation of the conjunctiva having a periodic seasonal incidence. Etiology It is considered a hypersensitivity reaction to some exogenous allergen, such as grass pollens. VKC is thought to be an atopic allergic disorder in many cases, in which IgE-mediated mechanisms play an important role. Such patients may give personal or family history of other atopic diseases such as hay fever, asthma, or eczema and their peripheral blood shows eosinophilia and inceased serum IgE levels. Predisposing factors 1. Age and sex. 4-20 years; more common in boys than girls. 2. Season. More common in summer; hence the name spring catarrh looks a misnomer. Recently it is being labelled as 'Warm weather conjunctivitis'. 3. Climate. More prevalent in tropics, less in temperate zones and almost non-existent in cold climate. Pathology 1. Conjunctival epithelium undergoes hyperplasia and sends downward projections into the subepithelial tissue. 2. Adenoid layer shows marked cellular infiltration by eosinophils, plasma cells, lymphocytes and histiocytes. 3. Fibrous layer shows proliferation which later on undergoes hyaline changes. 4. Conjunctival vessels also show proliferation, increased permeability and vasodilation. All these pathological changes lead to formation of multiple papillae in the upper tarsal conjunctiva. Clinical picture Symptoms. Spring catarrh is characterised by marked burning and itching sensation which is usually intolerable and accentuated when patient comes in a warm humid atmosphere. Itching is more marked with palpebral form of disease. Other associated symptoms include: mild photophobia, lacrimation, stringy (ropy) discharge and heaviness of lids. Signs of vernal keratoconjunctivitis can be described in following three clinical forms: 1. Palpebral form. Usually upper tarsal conjunctiva of both eyes is involved. The typical lesion is characterized by the presence of hard, flat topped, papillae arranged in a 'cobble-stone' or 'pavement stone', fashion (Fig. 4.20). In severe cases, papillae DISEASES OF THE CONJUNCTIVA 75 may hypertrophy to produce cauliflower like excrescences of 'giant papillae'. Conjunctival changes are associated with white ropy discharge. Fig. 4.20. Palpebral form of vernal keratoconjunctivitis. 2. Bulbar form. It is characterised by: (i) dusky red triangular congestion of bulbar conjunctiva in palpebral area; (ii) gelatinous thickened accumulation of tissue around the limbus; and (iii) presence of discrete whitish raised dots along the limbus (Tranta's spots) (Fig. 4.21). 3. Mixed form. It shows combined features of both palpebral and bulbar forms (Fig. 4.22). Vernal keratopathy. Corneal involvement in VKC may be primary or secondary due to extension of limbal lesions. Vernal keratopathy includes following 5 types of lesions: 1. Punctate epithelial keratitis involving upper cornea is usually associated with palpebral form of disease. The lesions always stain with rose bengal and invariably with fluorescein dye. 2. Ulcerative vernal keratitis (shield ulceration) presents as a shallow transverse ulcer in upper part of cornea. The ulceration results due to epithelial macroerosions. It is a serious problem which may be complicated by bacterial keratitis. 3. Vernal corneal plaques result due to coating of bare areas of epithelial macroerosions with a layer of altered exudates (Fig. 4.23). 4. Subepithelial scarring occurs in the form of a ring scar. 5. Pseudogerontoxon is characterised by a classical ‘cupid’s bow’ outline. Fig. 4.21. Bulbar form of vernal keratoconjunctivitis. Fig. 4.23. Vernal corneal plaque. Fig. 4.22. Artist's diagram of mixed form of vernal keratoconjunctivitis.c 76 Comprehensive OPHTHALMOLOGY Clinical course of disease is often self-limiting and usually burns out spontaneously after 5-10 years. Differential diagnosis. Palpebral form of VKC needs to be differentiated from trachoma with pre-dominant papillary hypertrophy (see page 67). Treatment A. Local therapy 1. Topical steroids. These are effective in all forms of spring catarrh. However, their use should be minimised, as they frequently cause steroid induced glaucoma. Therefore, monitoring of intraocular pressure is very important during steroid therapy. Frequent instillation (4 hourly) to start with (2 days) should be followed by maintenance therapy for 3-4 times a day for 2 weeks. Commonly used steroid solutions are of fluorometholone medrysone, betamethasone or dexamethasone. Medrysone and fluorometholone are safest of all these. 2. Mast cell stabilizers such as sodium cromoglycate (2%) drops 4-5 times a day are quite effective in controlling VKC, especially atopic cases. It is mast cell stabilizer. Azelastine eye drops are also effective in controlling VKC. 3. Topical antihistaminics are also effective. 4. Acetyl cysteine (0.5%) used topically has mucolytic properties and is useful in the treatment of early plaque formation. 5. Topical cyclosporine (1%) drops have been recently reported to be effective in severe unresponsive cases. B. Systemic therapy 1. Oral antihistaminics may provide some relief from itching in severe cases. 2. Oral steroids for a short duration have been recommended for advanced, very severe, nonresponsive cases. C. Treatment of large papillae. Very large (giant) papillae can be tackled either by : Supratarsal injection of long acting steroid or Cryo application Surgical excision is recommended for extraordinarily large papillae. D. General measures include : Dark goggles to prevent photophobia. Cold compresses and ice packs have soothing effects. Change of place from hot to cold area is recommended for recalcitrant cases. E. Desensitization has also been tried without much rewarding results. F. Treatment of vernal keratopathy Punctate epithelial keratitis requires no extra treatment except that instillation of steroids should be increased. A large vernal plaque requires surgical excision by superficial keratectomy. Severe shield ulcer resistant to medical therapy may need surgical treatment in the form of debridment, superficial keratectomy, excimer laser therapeutic kerateotomy as well as amniotic membrane transplantation to enhance reepithelialization.
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