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VERNAL KERATOCONJUNCTIVITIS (VKC) VKC is a chronic bilateral inflammation of the conjunctiva, commonly associated with a per- sonal and/or family history of atopy. More than 90 % of patients with VKC exhibit one or more atopic conditions such as asthma, eczema, or seasonal allergic rhinitis.

VKC is characterized by severe itching, foreign body sen- sation, thick stringy mucous discharge, photophobia and conjunctival injection.

Figure 2 – Cobblestone papillae in VKC

VKC may be subdivided into two varieties, palpebral and limbal. The classic conjunctival sign in palpebral VKC is the presence of giant papillae. They most commonly occur on the superior tarsal conjunctiva. Giant papillae are large, polygonal excrescences with flat tops, and are often described as “cobblestone papillae”. A mucous coa- ting may cover the giant papillae (Figure 2). In severe cases large papillae may cause mechanical ptosis

The limbal form of VKC commonly occurs in dark-skinned individuals such as those from Africa or India. As the name implies, papillae tend to occur at the limbus and have a thick gelatinous appearance. They commonly are associated with multiple white spots (Horner-Trantas dots), which are accumulations of degenerated epithelial cells and eosinophils (Figure 3).

Figure 3 – Horner-Trantas dots in VKC

The cornea may be affected in a variety of ways. Punctate epithelial keratopathy (PEK) may be due to the toxic effect of inflammatory mediators released from the con- junctiva. As the areas of PEK coalesce, they may result in

frank epithelial erosion resulting in a shield ulcer, which is typically shallow with white irregular epithelial bor- ders. It is pathognomonic of VKC (Figure 4).

Another type of corneal involvement is vernal pseudoge- rontoxon, which is a degenerative lesion in the periphe- ral cornea resembling corneal arcus.

Figure 4 – Shield ulcer in VKC

ATOPIC KERATOCONJUNCTIVITIS (AKC) AKC is a bilateral inflammation of the conjunctiva and eyelids, which has a strong association with atopic der- matitis. Atopic dermatitis is a common hereditary disor- der that usually starts in childhood; symptoms may regress with advancing age. Approximately 25 % of cases with atopic dermatitis may develop AKC.



AKC may affect eyelid skin and lid margins, conjunctiva, cornea, and lens. The skin of the eye- lids may exhibit eczematoid dermatitis with dry, scaly, and inflamed skin. Lid margins may show meibomian gland dysfunction and keratinization. Staphylococcal colonization of eyelid margins is very common and may result in blepharitis. The conjunctiva may show chemosis and typically a papillary reaction, which is more prominent in the inferior tarsal conjunctiva, in con- trast to that seen in vernal keratoconjunctivitis.

Hyperplasia of limbal regions may result in a gelatinous thickening, similar to the limbal variant of VKC. Fibrosis or scarring of the conjunctiva may result in symblepharon formation. Corneal involvement ranges from punctate epithelial keratopathy early in the course of the disease, to neovascularization, stromal scarring, and possibly ulce- ration.

Lenticular changes in AKC include anterior or posterior subcapsular cataract formation. Lens opacities are usual- ly bilateral and present in the second decade of life but progress very slowly. There may be an association with chronic use of topical corticosteroids.

Figure 5 – Atopic keratoconjunctivitis

GIANT PAPILLARY CONJUNCTIVITIS (GPC) GPC is an immune-mediated inflammatory disorder of the superior tarsal conjunctiva. As the name implies, the primary finding is the presence of “giant” papillae, which are typically greater than 0.3 mm in diameter (Figure 6). It is believed that GPC represents an immunologic reac- tion to a variety of foreign bodies, which may cause prolonged mechanical irritation to the superior tarsal conjunctiva. Although contact lenses (hard and soft) are the most common irri- tant, ocular prostheses, extruded scleral buckles, and exposed sutures following previous sur- gical intervention may precipitate GPC.

The best method of examining a patient who is suspec- ted of having GPC is, after removing their contact lenses if worn, to evert the upper lid to view the tarsal surface with a hand held magnifier. A drop of 2 % fluorescein is instilled into the cul-de-sac and the patient is asked to blink several times, then the lid is re-everted and exami- nation is performed with blue-cobalt light. Fluorescein will outline the giant 0.3 – 0.5 mm papillae. [5]

Another clinical sign of GPC may be chronic limbal vascu- larization due to hypoxia associated with prolonged and persistent use of contact lenses.

Figure 6 – Giant papillae in the tarsal con- junctiva of a chronic contact lens wearer which are not taking the cobble-stone appearance as in VKC



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