Understanding the ocular allergic response and the clinical presentation of the different forms of allergic conjunctivitis will help you manage these sometimes incapacitating disorders. That said, let's look at five ocular allergic diseases, starting with the most common: Seasonal allergic conjunctivitis (SAC) and perennial allergic conjunctivitis (PAC).

Seasonal vs. perennial

The most significant differences between seasonal and perennial allergic conjunctivitis - as their names imply - is that the former occurs during specific times of the year and the latter is a chronic condition.

In SAC, symptoms are triggered by specific pollens, such as ragweed or grass pollen. In PAC, symptoms can occur year-round in individuals with sensitivities to allergens, such as dust mites or cat dander.

Symptoms of SAC and PAC include bilateral itching, tearing, burning and mucus discharge, often accompanied by sneezing and rhinitis. Signs of SAC and PAC can be virtually absent or consist of varying degrees of conjunctival redness and edema. Corneal involvement, however, isn't present in either type of conjunctivitis.

SAC and PAC are characterized by type I hypersensitivity reactions. (For more on reactions and types, see "Hypersensitivity Defined" and "Two Types of Reactions" on page 4.) Type I hypersensitivity reactions are also called immediate hypersensitivity reactions because the allergic response occurs within minutes of allergen exposure. But this immediate reaction (early phase) can be followed by a late-phase reaction of signs and symptoms up to 8 hours later. The mediators released from the degranulation of mast cells in the early phase aid in eosinophil infiltration of the conjunctiva in the late phase. The eosinophils in turn release mediators, such as major basic protein (MBP), that are responsible for further mast cell degranulation resulting in the late-phase symptoms. The cellular infiltration of eosinophils in the late-phase reaction has been demonstrated in conjunctival scrapings from patients with SAC and PAC.

If your patient has other allergic disorders, such as eczema, hay fever and asthma, and a family history of atopy, this will help you establish the diagnosis of SAC or PAC. Fluctuations of symptoms in SAC and the chronic year-round symptoms of PAC will help differentiate the two types.

Symptoms of other ocular conditions, such as blepharitis, can mimic those of SAC and PAC. However, patients with blepharitis typically present with burning, crusting and redness of the lid margins without the itching commonly observed in ocular allergy. Conjunctival scrapings of the eye can also be performed for a definitive diagnosis. An abundance of eosinophils would indicate SAC or PAC.

Your first course of action when treating SAC and PAC is to instruct patients to avoid the causative allergen. When this isn't possible, then adjuvant therapy is necessary. Patients with allergic disorders, such as hay fever, often benefit from immunotherapy, but it's less effective for patients with ocular allergy.

Other therapeutic options like topical vasoconstrictors, such as naphazoline HCI, and topical antihistamines such as emedastine and levocabastine, help treat mild to moderate cases of SAC or PAC. But a combination of topical antihistamines and vasoconstrictors is more effective than either drug alone in providing greater relief. Severe cases may require oral antihistamines, but the sedating effects of these drugs make them less desirable.

Mast cell stabilizers, such as pemirolast potassium (Alamast), are effective in treating SAC and PAC, and they don't dry the eyes like oral and topical antihistamine drops. Pemirolast potassium prevents mast cell degranulation and can be taken up to four times a day. Recent studies demonstrate efficacy with b.i.d. dosing. Because mast cell stabilizers inhibit the release of inflammatory mediators, they're used primarily to prevent symptoms. They relieve symptoms throughout the season or all year long if the patient suffers from PAC.

With caution, you can prescribe a short course of topical steroids in severe cases. You can use topical steroids concurrently with other allergy medications, such as pemirolast potassium, which can be continued after discontinuing steroid use.

Youth affected

Vernal keratoconjunctivitis (VKC) is an uncommon, chronic, bilateral, ocular inflammatory disorder that affects mostly children and young adults. It can cause severe damage to the cornea, resulting in loss of vision. VKC is more common in boys than in girls and occurs more frequently in patients with a history of atopy. It's more prevalent in warmer climates, such as the Mediterranean area, Africa and India.

In children, the disease typically lasts 4 to 10 years.

The main symptoms of VKC include burning, itching, mucous discharge, tearing, foreign body sensation, photophobia and conjunctival injection.

The three main clinical types of VKC are:

> Palpebral VKC. In this type, giant papillae form on the superior tarsus (see above). The papillae tend to be flat-topped and polygonal in appearance, resembling cobblestones.

> Limbal VKC. This type is characterized by mucoid nodules that form on parts or all of the limbus. White dots called Homer's points or Trantas' dots appear around the limbus; these dots are clumps of eosinophils with dead epithelial cells (see left).

> Mixed VKC. This type has components of both palpebral and limbal VKC. The cornea also may be involved with the presence of punctate epithelial keratopathy, which can progress to form a shield ulcer. Pseudo-gerontoxon is another degenerative change of the cornea that resembles an arcus senilis, which often occurs in VKC. There's also a higher incidence of keratoconus in VKC patients.

VKC is a type I and a type IV hypersensitivity reaction. This is evident by the histopathology of the conjunctiva, characterized by an increase of not only mast cells and eosinophils but also Tcell lymphocytes. These T-cells interact with macrophages, which are also found in increased numbers in the conjunctiva. This overabundance of inflammatory cells contributes to giant papillae formation.

Furthermore, the inflammatory mediators released by these cells can lead to the corneal involvement frequently observed in patients with VKC. The release of MBP and eosinophil cationic proteins by eosinophils during degranulation have been implicated in the damage of the corneal epithelium.

How do you differentiate VKC from other ocular allergic diseases? First, SAC and PAC lack corneal involvement and giant papillae formation, so you can easily differentiate VKC from these two disorders. Lid scrapings also will reveal a greater cellular infiltration in patients with VKC than in SAC and PAC.

Second, although contact lens-associated giant papillary conjunctivitis (GPC) may have a similar clinical appearance to VKC, it's invariably associated with contact lens wear.

And third, atopic keratoconjunctivitis (AKC) also presents with a papillary reaction, but unlike VKC, it affects predominantly the lower fornix. The patient population affected with AKC also tends to be older than that of VKC. These patients also invariably have atopic dermatitis. Furthermore, AKC more commonly exhibits conjunctival cicatrization and corneal vascularization, which are very rare for VKC.

Patients can reduce symptoms of VKC by avoiding the causative allergen. But this is often too difficult for most patients. Topical mast cell stabilizers like pemirolast potassium can be more effective in treating VKC, and can be used chronically. Topical antihistamines and vasoconstrictors also can be used for relief, but they tend to be less effective than mast cell stabilizers.

Patients with severe symptoms may require topical corticosteroids, but avoid long-term use to minimize adverse effects associated with their use. Patients with a shield ulcer may need a bandage contact lens.

Atopic dermatitis complication

AKC typically affects patients with atopic dermatitis. Like VKC, it occurs more frequently in men than in women. It's a bilateral, potentially blinding keratoconjunctivitis that presents in the late teens or early 20s and can persist for many years. Patients commonly complain of itching, burning, tearing and a mucous discharge. The lids are red, thickened, macerated and sometimes fissured.

Associated chronic blepharitis is a common finding in AKC. Conjunctival involvement affects primarily the inferior forniceal and tarsal conjunctivae. During exacerbations, papillary hypertrophy on the lower tarsal conjunctiva can occur, differentiating it from VKC. In severe cases, cicatricial conjunctivitis can result with the formation of symblepharon in the inferior fornix. Corneal involvement is the main cause of visual impairment in AKC. Punctate epithelial defects are common corneal findings, which may progress into epithelial defects and ulceration. In severe cases, you may observe neovascularization of the cornea and stromal scars.

Several ocular conditions have been associated with AKC. For example, herpes simplex keratitis and staphylococcus superinfections are seen more frequently in AKC patients. Keratoconus, presenile cataracts and a rare retinal detachment may also be associated with this disease (see below).

Like VKC, AKC is characterized by a type I and a type IV hypersensitivity reaction. Thus, the histopathology of the conjunctiva demonstrates infiltration of the cells characteristic of these two types of reactions, for example, numerous mast cells, basophils, eosinophils, macrophages and T-cell lymphocytes. The release of mediators by the inflammatory cells is responsible for the signs and symptoms of the disease.

Although similar to SAC and PAC, AKC symptoms are usually much more severe. Lid involvement and a papillary response of the lower tarsal conjunctivitis differentiates AKC from VKC. In addition, VKC typically affects a younger patient population than AKC.

Treating AKC is similar to VKC. Again, although topical vasoconstrictors and antihistamines may be used, topical mast cell stabilizers, such as pemirolast potassium and nedocromil sodium, tend to be more effective in reducing the signs and symptoms of AKC. The topical application of steroids may be used for a short time for acute inflammatory flares. Therapy with antivirals for herpes simplex keratitis and with antibiotics for staphylococcal infection may also be necessary.

Contact lens connection

GPC is a fairly common condition among contact lens wearers. It occurs more often in people who wear soft lenses than those who wear gas permeable lenses. Sutures from cataract surgery and ocular prostheses also can cause GPC. It's believed that patients with atopic diseases such as asthma or hay fever are at increased risk of GPC.

Symptoms can start months to years after beginning contact lens wear. These include ocular itching, blurred vision, increased mucus production and contact lens intolerance. Patients also may complain that the lens is being pulled up by the upper lid into the upper fornix. Signs consist of giant papillae on the upper tarsal conjunctiva, which may resemble VKC and conjunctival injection (see above). The conjunctiva overlying the giant papillae is frequently thick and irregular.

The etiology of contact lens-associated GPC is unclear. However, it's likely associated with the lens material, the lens solutions, an immune response to the lens or irritation due to trauma of the tarsal conjunctiva.

GPC involves both a type I and a type IV hypersensitivity reaction. As in AKC and VKC, the histopathology of the conjunctiva in GPC demonstrates a cellular infiltration of eosinophils, mast cells, macrophages and T-cell lymphocytes. The inflammatory mediators released by these cells are responsible for the giant papillae formation and symptoms of GPC.

The diagnosis of GPC is usually straightforward. A contact lens wearer with itching and lens intolerance and demonstrating giant papillae on examination should raise the index of suspicion. The lack of corneal involvement also can help differentiate GPC from VKC. GPC is occasionally confused with SAC or PAC, especially if the disease isn't fully developed. But a good history and careful slit lamp examination should lead to the correct diagnosis.

Although treating GPC consists of discontinuing contact lens use, most patients want to continue wearing them. Therefore, therapy zeros in on good lens hygiene, minimizing lens wear, changing lens fit to avoid mechanical trauma to the tarsal surface and using disposable lenses.

Gas permeable lenses are less likely to cause GPC than soft lenses. However, if the patient suffers from severe symptoms, he should discontinue lens use until the syndrome has resolved. Topical steroids aren't typically used to treat GPC. But the patient may apply a topical mast cell stabilizer, such as nedocromil sodium, or a second-generation mast cell stabilizer, such as pemirolast potassium, which contains glycerin in its formulation.

Differentiating the itch

Healthcare practitioners frequently encounter ocular allergies. Knowing the clinical presentation and understanding the underlying immune mechanism of the different subcategories of ocular allergy is important for managing the diseases.

SAC, PAC and GPC are usually less severe than VKC or AKC, and rarely have permanent sequelae: In contrast, VKC and AKC, although less common, can be potentially blinding. Therefore, it's important to diagnose the disease in a timely manner and encourage the patient to use the medications as directed.

By Sharon K. Sra, M.D., and Stefan Trocme, M.D.

Dr. Sra is a research fellow at the Eye Research Laboratory at the University of Texas, Medical Branch (UTMB) in Galveston, Texas. Dr. Trocme is an associate professor and vice chairman of the department of ophthalmology, director of corneal and research services and director of the eye research laboratory at UTMB.

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