CLINICAL CHALLENGES with Eric Schmidt, O.D.
The Uncommon Allergy
How to recognize vernal keratoconjunctivitis.

Allergic eye disease is one of the most common problems we see. But not all allergies present as "itchy, burny" seasonal allergic conjunctivitis. Some take on a more painful and serious form.

The case

Jason was a 22-year-old student whom I'd seen a few times previously. He was a high hyperope with an accommodative esotropia who'd worn disposable soft contact lenses for 8 years. During that time he'd had two episodes (that I knew of) of giant papillary conjunctivitis (GPC). I had treated them acutely with a short regimen of fluorometh-olone (FML), followed by longer courses of cromolyn sodium (Crolom) OU b.i.d. Both times, Jason was able to resume daily contact lens wear.

Jason told me that he'd also been treated for allergic conjunctivitis by other doctors at least three times. Despite these problems, he was still happy wearing contact lenses.

But what brought Jason in this time was different. "My eyes have never felt like this before," he said.

A new problem

When he'd awakened 2 days earlier, his right eye was sore and red, with some itching. It teared a great deal, but the left eye felt fine. Jason had slept in his contact lenses that night (as he occasionally did) and removed them in the morning. He tried to put a new contact lens in his right eye, but the pain increased so he took it out. Over the 48-hour period, his eye continued to tear and hurt, and mucous discharge developed. The eye was redder and moderately photophobic when I saw Jason. He wasn't taking medication and denied trauma or excessive rubbing.

The exam

Jason's unaided visual acuity OD was 20/400. This improved to 20/30 with pinhole occlusion. The visual acuity OS with his contact lens was 20/50, which didn't improve with refraction or pinhole because of amblyopia. External tests were normal, except for a 15 prism diopter esophoria on cover testing.

With a slit lamp I found a great deal of surface inflammation OD. His lids showed mild mucous accumulation, but the meibomian glands weren't capped. The bulbar conjunctiva OD exhibited 2+ injection but the redness was more severe at the superior limbus. I saw a great deal of limbal vessel engorgement superiorly.

Upon eversion of the right upper lid, 2-3+ giant papillae became evident. I noted 1+ papillae in the lower palpebral conjunctiva. The cornea appeared to have some stromal haze superiorly OD. I instilled sodium fluorescein into that eye and rather than showing edema, the dye revealed a frank epithelial corneal defect in that area.

The area of staining was demarcated from the limbus and had sharp borders. No infiltrates were associated with the lesion. The anterior chamber was well formed and quiet.

Slit lamp examination of Jason's OS was relatively normal, except for 1+ papillae on the upper palpebral conjunctiva. His contact lens fit well and didn't move excessively.

Infection, allergy or overwear?

This, obviously, wasn't routine seasonal allergic conjunctivitis (SAC). Given Jason's history of sleeping in contact lenses plus a corneal defect, I was concerned about an infectious ulcer. I ruled this out based on the clinical appearance of the lesion.

Though large, it didn't seem to be infectious. I saw no infiltrates, and the borders were sharp, not ragged, as seen in infectious corneal ulcers. The dye didn't seep under the borders of the lesion; it stayed within the confines of the defect, consistent with a structural etiology.

Discharge from infectious ulcers is purulent. The discharge from Jason's lesion was sparse and stringy. This lesion was also separated from the limbus and had no associated iritis. But my biggest clue was the large papillae on the upper lids OU. Giant papillae associated with Jason's symptoms are consistent with vernal keratoconjunctivitis (VKC). The corneal defect was a shield ulcer, which is common with VKC.

The making of VKC

VKC, or vernal catarrh, is a more severe allergic conjunctivitis. Like SAC, VKC is a type I allergic reaction marked by a rapid, exaggerated hypersensitivity response. It shares many characteristics of SAC, including itching, redness and papillae. But unlike SAC, it exhibits more chronic forms of inflammation. These chronic components can lead to ocular changes and vision loss if not treated appropriately.

VKC is more common in warmer climates and younger patients. Though it can present any time, it tends to be seasonal, appearing most in spring and fall. It's typically bilateral, and its symptoms are more exaggerated than those of SAC.

Hallmarks of VKC

The hallmark of VKC is giant papillae, which cause most of the symptoms and are usually present only on the upper palpebral conjunctiva. You'll need to evert the lids to see them. They produce the mucous discharge, and the associated mast cell destabilization causes inflammation of the ocular surface. Papillae can become so large that they create a pseudoptosis of the upper lid.

Intensified inflammation can affect the cornea, as happened in Jason's case. A diffuse superficial punctate keratitis (SPK) is the most common corneal response, but a shield ulcer can form. Some experts feel that these shield ulcers develop from mechanical disruption of the corneal epithelium because of direct contact and extended rubbing by the giant papillae. Others feel that the epithelial breakdown is strictly inflammatory. Whatever the etiology, you must treat a shield ulcer quickly.

Making Jason comfortable

Because VKC is an inflammatory disease, 3 to 4 weeks of a topical steroid is the best treatment. However, the shield ulcer complicated Jason's case. It wasn't infectious yet, but an exposed corneal epithelium means a risk of secondary infection.

I set these treatment goals:

• prevent infection
• relieve Jason's symptoms
• quell the inflammation.

I prescribed tobramycin/dexamethasone (TobraDex) OD q.4.h. and recommended cold compresses to make him feel better. Of course, I asked him to discontinue wearing the contact lenses for at least 1 month.

Three days later, the shield ulcer was 90% resolved. Jason felt "100% better," even though the papillae were still there. They were much less red and inflamed, however. I had Jason decrease the tobramycin/ dexamethasone to q.i.d. for 1 more week and continue the cold compresses.

At his next visit, Jason said that his eyes felt normal and had no more discharge. He still had 1-2+ papillae under his upper lids OU, but the inflammatory appearance and the shield ulcer were gone. I had him taper the tobramycin/dexamethasone rapidly. Now I had to attack the papillae to prevent recurrences.

An eye to the future

Mast cell stabilizers are the most effective agents against papillae. Because Jason had responded well to cromolyn sodium before, I prescribed it OU q.i.d. for the next 3 months, until allergy season was over. I also told him not to wear contact lenses for that period. After that, I hope he'll be able to resume wearing them on a semi-regular basis. I'm also going to prophylactically put Jason on cromolyn sodium for 4 months starting next March to try to prevent a recurrence.

Contributing Editor Eric Schmidt, O.D., is director of the Bladen Eye Center in Elizabethtown, N.C. E-mail him at KENZIEKATE@aol.com.