Pacific Optometry Continuing Education Ocular Allergies Goodwin

Ocular allergy is a common condition affecting approximately 17 to 20% of the population, and its incidence is increasing.(1,2,3) The conjunctiva is exposed to many environmental allergens and is often the location of first contact with an allergen. For this reason, the management of ocular allergies is a very important aspect of many vision care practices.

Allergic ocular surface disease is traditionally divided into five categories, all of which result from a hypersensitivity reaction by ocular tissues to one or more allergens.

Chronic allergic diseases with the potential for causing significant ocular consequences include:

Atopic and vernal keratoconjunctivitis are potentially vision-threatening conditions due to the risk of corneal ulceration, vascularization, and scarring. (4)

Although SAC (also known as hay fever conjunctivitis) is less severe than other ocular allergies, it is by far the most common type of allergy affecting the eyes.(5,6) SAC typically occurs in the fall and spring when grass, tree, or ragweed pollens are abundant. In contrast, PAC can occur year-round, and its causes can include animal dander, insects, and dust mites.

SAC and PAC can occur at any age, but patients are typically young, with an average age of 20 to 30 years.(5,6,9) The incidence of sensitivity to airborne allergens typically begins around age 8 to 10 years of age.(10) Eighty percent of people who will develop allergies have symptoms before the age of 20 years.(11) There is no statistical difference in the number of females versus males affected by seasonal and perennial allergies.(8,9,12)

SAC and PAC do not typically threaten vision, but they do alter the quality of life, cause missed workdays, and inflict a significant social and financial burden on patients.(7)

Ocular allergy symptoms can result in patient discomfort that interferes with visual tasks such as computer work and recreational activities. Twenty percent of allergy suffers report taking time away from work due to allergy symptoms.(8) Direct and indirect costs of SAC and PAC include lost wages as well as physician and medication costs.(7)

Exposure to environmental allergens, such as cigarette smoke and pollution, has been associated with the development of ocular allergies to other allergens.(10) Children born by Caesarean section (13) and those who were fed milk other than breast milk during the first 4 months of life (10) also have an increased risk of developing allergies. Dietary intake of n-6 polyunsaturated fatty acids has also been associated with seasonal rhinoconjunctivitis.(14)

Vernal keratoconjunctivitis is rarer than SAC and PAC, but due to cornea involvement, it is potentially a more serious condition. VKC has a mean age of onset of 7 years and the majority of cases (85%) have an onset prior to age 10 years.(16) For this reason, an initial diagnosis of VKC in an adult patient should be suspect.(5)

VKC is found most commonly in males (6,15) and is most likely to occur in warm, windy climates such as the Mediterranean, West Africa, Japan, India, and South America.(17,18) The condition is not as common in North America and Western Europe (17); however, the migratory nature of populations accounts for an increased prevalence of the disease in these countries.(18)

Atopic keratoconjunctivitis, which is an allergic conjunctivitis associated with atopic dermatitis, is the most potentially blinding of all of the ocular allergies.(1) Like vernal, AKC is more common in males. The condition typically begins in the late teens or early twenties with a peak severity occurring between ages 30 to 50 years.(19) Patients with AKC typically have eczema on the eyelids and skin as well as a history of asthma.

Approximately 15 to 40% of patients with atopic dermatitis will develop AKC (17), and at least 95% of patients with AKC have eczema.(19) Eczema typically starts in childhood and ocular symptoms occur somewhat later in life.(20)

With the use of disposable contact lenses, GPC has become a far less frequently occurring allergy. GPC most commonly develops after prolonged conjunctival contact with a foreign substance such as a contact lens. It has also been reported with exposure to ocular sutures or prostheses.

Often it is not the contact lens itself that causes GPC, but rather it is deposits or allergens on the surface of the contact lens. These allergens are rubbed against the upper palpebral conjunctiva many times during the day and this causes sensitization.

GPC can occur in patients who wear either hard or soft contact lenses, but soft lenses cause GPC more commonly than rigid contact lenses. This is due to the ability of soft contact lenses to accumulate more deposits than rigid lenses. Also, the larger surface area of a soft lens produces a larger area of reaction. People who sleep in their lenses are three times as likely to develop GPC as those who do not.

Patients typically consider ocular problems including itch, watering, and redness to be the most important symptoms requiring relief.(21) However, these symptoms are often overlooked by non-eye care practitioners, and many physicians minimize the effects that allergies have on their patient’s comfort and well-being.(22)

A large number of patients self-medicate to reduce their symptoms, and, as a result, many of them are not treated fully or appropriately.

An understanding of basic immunology will aid in proper diagnosis and appropriate management of patients with ocular allergies.

Mast cells are primarily responsible for the hypersensitivity reaction that occurs in SAC and PAC. In addition to mast cells, eosinophils and T lymphocytes are also involved in VKC, AKC, and GPC.

Allergy symptoms occur after an allergen binds to immunoglobulin E (IgE) on conjunctival mast cells in a sensitized individual. This causes mast cell degranulation, which releases inflammatory mediators such as histamine, leukotrienes, prostaglandins, tryptase, and cytokines.(23,24) These mediators trigger the acute, or early phase, of an allergic reaction. Histamine induces itching, redness, and swelling. Prostaglandins and leukotrienes are responsible for increased mucus secretion and vascular permeability.

Large doses of an antigen can cause the initial allergic reaction to progress to a late-phase response.(25) Eosinophils and T lymphocytes are responsible for this late-phase reaction. T helper 2 (TH2) cytokines, including interleukin (IL)-4, IL-5, IL-6, IL-8, IL-13, stem cell factor, platelet activating factor, and tumor necrosis factor (TNF) can trigger a series of inflammatory events.

These events, including the expression of chemokines, protein regulated on activation normal T-cell expressed and secreted (RANTES) monocyte chemoattractant protein-1 (MCP-1), eotaxin, intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM), and p-selectin lead to the recruitment of eosinophils and neutrophils. This can result in allergy symptoms that persist for up to 24 hours.(23,26)

Itching is the hallmark symptom of ocular allergies. Without itching, any diagnosis of ocular allergy is suspect. Itching with SAC and PAC is typically greater than the ocular signs would suggest.(27,28) Because the eyes itch, patients typically rub them, but this only exacerbates the signs and symptoms of allergic conjunctivitis.(29)

In addition to itching, SAC and PAC can also present with bilateral redness, burning, tearing, photophobia, and occasionally stringy mucous discharge. Swelling of the eyelids is usually present, and the eyes will have a glassy look due to conjunctival swelling. (See Figure 1.) The ocular symptoms of SAC and PAC are reoccurring and are exacerbated during pollen season or in the presence of specific antigens.

Patients with SAC usually have a family or personal history of food or environmental allergies including PAC, asthma, or eczema.(8,30) Although the eye may be the only organ involved, nasal symptoms and sneezing are also frequently reported.

Patients with SAC often present with mild to moderate conjunctival injection and chemosis as seen in Figure 1. Chemosis is usually more prominent in the nasal conjunctiva because the conjunctiva is more loosely attached in this area.(31) Swelling of the eyelids may cause a narrowing of the intrapalpebral fissure, and papillae may be present on the palpebral conjunctiva.

Because of the potential for vision loss, it is critical that the acute forms of ocular allergies such as SAC and PAC are correctly differentiated from sight-threatening ocular allergies such as VKC and AKC.

Allergens that cause VKC are similar to those that cause SAC, and a hyper-reaction to histamine has been found in VKC patients. It has been shown that VKC patients have a more intense reaction to lower histamine doses.(6)

The most common sensitizing agent producing VKC is rye grass (15) with other common causes being pollen, dust mites, and animal dander.(6,18) Non-specific factors such as sun, dust, and wind exposure can also trigger the onset of VKC.(32)

Bilateral intense itching is characteristic of VKC, but tearing, photophobia, blepharospasm, blurred vision, stringy discharge, and difficulty opening the eyes in the morning are also commonly reported. Patients might also report pain if there is corneal involvement.

VKC patients typically have seasonal exacerbations, but at least 60% of them have recurrences year-round.(15) For those with seasonal exacerbations, the most severe appearance of the disease usually occurs in the spring.(15) Approximately 16% of patients with seasonal exacerbations progress to experiencing perennial VKC symptoms.(15)

Nearly 49% of patients who suffer from VKC have a family history of atopic disease such as asthma, rhinitis, or eczema. VKC is also commonly associated with a personal allergy history, which might include asthma, rhinitis, or atopic eczema.(15)

Giant papillae on the superior palpebral conjunctiva are the clinical hallmark of VKC. (See Figure 2.) In severe VKC, the papillae are often greater than 1.0 mm in diameter giving them a cobblestone appearance. These large papillae can result in pseudoptosis.

Papillae can also occur in the limbal area, and these limbal papillae are more common in non-Caucasians. The limbal papillae that have a white, chalky area at the apex are known at Trantas’ dots or Horner’s points. (See Figure 3.) They contain a high concentration of eosinophils and degenerating epithelial cells. The limbus can become inflamed causing the circumference of the limbus to appear opaque all around the cornea. Peripheral neovascularization can also occur.

Papillae are found solely on the tarsal conjunctiva in 83 to 84% of VKC patients. Bulbar papillae are present in 7% of cases, and 9 to 17% of VKC patients have both forms of papillae.(15,33) Cobblestone papillae are found in approximately 16% of cases.(15)

Ninety-eight percent of VKC presentations are bilateral (15), but the presentation severity can be asymmetric.(5)

Corneal complications are common in patients with VKC. Early signs of corneal involvement include punctate erosions, which can coalesce to form macroerosions that can be quite painful. Inflammatory debris often accumulates in the macroerosion forming an opaque plaque, which can prevent epithelialization of the cornea and thus cause scarring.

These non-healing epithelial defects, also known as shield ulcers, are typically oval in shape and located superiorly. Ulcers make the eye more susceptible to secondary infections, especially when the VKC is treated with topical steroids. Other complications of shield ulcers can include corneal vascularization, corneal opacification, strabismus, and amblyopia in children.

It is thought that corneal damage producing shield ulcers might be due to eosinophil granule major basic protein (MBP) substance. Large amounts of MBP have been found in tears and ocular tissues of VKC patients, and this substance can damage tissue and slow wound repair.(1) It has also been hypothesized that shield ulcers can be caused by mechanical abrasion of the cornea, possibly due to eye rubbing.(35)

Tanaka, et al., (36) found that the degree of hyperemia and chemosis is related to the severity of corneal complications in patients with VKC and AKC. They also found that papillae height and the amount of discharge did not predict the severity of the corneal complications. This suggests an inflammatory mechanism rather than a mechanical role in corneal damage associated with VKC and AKC.

Symptoms of AKC include intense bilateral itching of the eyelids and conjunctiva. Tearing, burning, foreign body sensation, photophobia, and stringy, ropy discharge are also typically present. Although some patients experience exacerbations in the winter and summer months, symptoms are usually present year-round.

When considering the possibility of AKC, it is essential to obtain a thorough personal and family history of allergic disease. Up to 60% of AKC patients have a family history of allergies, and approximately 92% will report a personal occurrence of non-ocular allergies.(16) At least 95% will have eczema, and 87% have asthma.(19)

Checking for signs of eczema is necessary when examining patients with AKC. The systemic manifestations of atopic dermatitis can help to differentiate this condition from VKC.

Due to eczema in the periorbital area, the eyelids tend to be thick, indurated, and red. Ptosis is often present. Chronic blepharitis, meibomian gland dysfunction, and dry eye have also been associated with AKC.(20)

Papillary hypertrophy of the upper, and, more commonly, the lower palpebral conjunctiva is a common finding in AKC patients. Hyperemia and chemosis, which are most prominent in the inferior and palpebral conjunctiva, will also be evident. In addition, gelatinous nodules with or without Tranta's dots might be present.(19,20)

Due to corneal involvement and other ocular manifestations, AKC can have dramatic effects on a patient’s vision. Corneal complications commonly occur and punctate keratitis can be seen early in the development of this condition.

Prolonged inflammation can cause persistent epithelial defects and plaque formation. Microbial infection, corneal ulceration, neovascularization, and superior pannus can also result. (See Figure 4.)

Keratoconus and atopic anterior subcapsular cataract formation is common in AKC patients.(19) Posterior subcapsular cataracts and glaucoma can also result from long-term steroid use. It is thought that persistent eye rubbing results in an increased risk of retinal detachment.

The most common cause of GPC is an allergic reaction to protein deposits on contact lenses. Both a mechanical and an immunologic process have been suggested as the reason for hypersensitivity to theses deposits. The time of onset between a soft contact lens fitting and the onset of GPC is usually between 10 to 20 months for patients who will experience this problem.(37) The condition is most often bilateral but can be asymmetric; only 10% of cases are unilateral.(37)

A coated or poorly fitting contact lens can produce trauma to the tarsal conjunctiva, which aids in development of GPC by allowing allergens on the contact lens to be exposed to the immune system. Immunological cells, e.g., mast cells and eosinophils, are present and IgE is found in the tears of patients with GPC.

GPC can occur with any type of contact lens including high Dk silicone hydrogel contact lenses. Lenses that have a higher water content (e.g., US Food and Drug Administration type 2 and 4 lenses) tend to have more deposits and lenses that are ionically charged (e.g., US Food and Drug Administration type 3 and 4 lenses) also tend to attract more proteins. Type 4 lenses seem to develop the most protein deposits.(37)

Symptoms of GPC include itching, foreign body sensation, blurred vision, increased mucus production, and contact lens intolerance. Patients will also often complain about mucus in the nasal canthus, especially upon wakening. Symptoms are not as severe as for VKC, but the appearance can be similar to advanced cases of GPC.

Patients with GPC are more likely than others to have environmental allergies, and those who do have environmental allergies typically have more severe GPC symptoms as compared to those who do not.(37)

The appearance of GPC is similar to that of VKC, but vision loss does not occur with GPC. In part, this may be due to a lower level of a cytotoxic mediator called eosinophil cationic protein (ECP) in the tears of GPC patients as compared to those with VKC.(1)

GPC patients commonly present with papillae greater than 0.3 mm in diameter on the superior tarsal conjunctiva. The papillae have a central blood vessel, and the tips stain with sodium fluorescein. In soft contact lens wearers, papillae form near the upper edge of the tarsal conjunctiva. In contrast, papillae form nearer the eyelid margin in rigid contact lens wearers.(37)

Two types of papillae patterns have been described in high Dk silicone hydrogel contact lens wearers. The first is a generalized pattern in which papillae cover the entire surface of the palpebral conjunctiva. The second pattern is localized to one or two areas of the palpebral conjunctiva, typically near the eyelid margin.

The corneal epithelium does not become involved in GPC, so serious complications are not usually caused by this allergy.

The diagnosis of ocular allergies is most often made clinically, however special diagnostic testing can be helpful in some cases.

The "skin-prick test" is an inexpensive way to provide supportive evidence of allergies. This test can also aid in identifying the specific allergen causing the patient's problem, and this can be helpful in avoiding the offending agent. The test is sensitive for systemic allergies, but it is positive in only 20% of patients with ocular allergies.(38)

During the test, allergens such as pollen, dust mite extracts, or animal dander are applied to the forearm or back by making shallow pricks with a lancet or a needle. Saline is used as a negative control, and histamine is used as a positive control. A skin wheal 2.0 mm or greater in diameter occurring within 15 minutes of exposure is considered a positive test result and indicates that the patient is responsive to the allergen.(22)

In the conjunctival provocation test (CPT), allergens are applied topically into the conjunctival sac. The presence of chemosis, hyperemia, and itching within 20 minutes of instillation is considered a positive response.(22) CPT is inexpensive and easy to perform.

Cytology specimens can be obtained from the conjunctiva, stained, and examined microscopically for the presence of eosinophils and mast cells. Eosinophils are not usually present in patients without allergies but are present when an allergic reaction is occurring. Therefore, the presence of eosinophils is considered diagnostic of allergy.(5,22)

Eosinophils are present during the active phase of VKC, but may be absent following anti-allergy treatment or during the inactive phase of VKC. The presence of mast cells is also highly indicative of active allergy.(22)

Tear fluid analysis can also be performed. A level of IgE in the tears greater than 16 iu/ml is indicative of allergic conjunctivitis. Tryptase, histamine, leukotrienes, and certain cytokines have also been found to be increased in the tears of patients with ocular allergies.(6,17,22)

Analysis of the tears does not differentiate between different types of ocular allergies.

Differential diagnoses for patients with suspected ocular allergies should include dry eye, blepharitis, infectious conjunctivitis, subconjunctival hemorrhage, and uveitis. Itching is indicative of an allergy, especially if it occurs in the spring or fall. Burning, tearing, and foreign body sensation are commonly caused by dry eye or blepharitis. Crusting of the lashes is typically present with blepharitis. Bacterial conjunctivitis typically produces a purulent discharge, and patients report the eyelids being stuck together, especially upon awakening. Painful preauricular lymph nodes and watery discharge indicate a viral conjunctivitis. A painless, focal area of solid redness over the sclera would indicate a subconjunctival hemorrhage. Uveitis presents with pain, photophobia, and circumcorneal injection.

Treatment options for ocular allergies include non-pharmacological and palliative options, topical medications, oral medications, and immunotherapy. The choice of treatment will depend on the severity of the condition as well as medication cost and expected patient compliance.

Non-pharmacological treatment including allergen avoidance, cold compresses, and artificial tears can provide short-term relief for allergy symptoms. For example, avoidance of allergens can result in up to a 30% decrease in symptoms.(40) However, removal of the offending agent may not be possible. Hospitalization might be necessary to stabilize severe cases of VKC if allergen avoidance is not possible.

Avoiding allergens can involve some difficult lifestyle changes such as removal of pets, avoiding activities that patients enjoy, or even moving to a location with different environmental conditions.

Use of cold compresses can reduce vasodilatation and provide temporary symptomatic relief. Artificial tears used 2 to 4 times daily can also aid in removal and dilution of allergens and can provide ocular lubrication.

Use of systemic antihistamines can cause drying of the ocular surface and exacerbate ocular allergy symptoms. Artificial tears should be recommended in conjunction with these agents.

Topical medications provide ease of use, rapid drug delivery and absorption, and decreased systemic side-effects.(41) These medications act directly at the site of application, e.g., the eyes, but ocular application has also been shown to relieve nasal allergy symptoms.(42) It is thought that this occurs due to drainage of the medication through the nasolacrimal duct to the nose.(20) Absorption through the nasal mucosa is also responsible for producing systemic side-effects.

Vasoconstrictors, antihistamines, mast cell stabilizers, non-steroidal anti-inflammatory drugs (NSAIDs), and mild steroids are all effective in managing ocular allergic conjunctivitis. Each drug category acts at a different stage in the inflammatory/allergy process.

Vasoconstrictors are sympathomimetic agents that are readily available over-the-counter. Alone, they are effective at reducing redness, but they have no direct effect on the allergic response itself.(41) For this reason, these agents are often combined with an antihistamine, which relieves itching.

Adverse reactions to vasoconstrictors can include burning and stinging on instillation and mydriasis.(41) Long-term use of topical vasoconstricting agents is not recommended due to the possibility of rebound conjunctival hyperemia.(26)

Activation of H1 histamine receptors stimulate itching, whereas H2 receptors are involved in vasodilation.(41,44,45) Topical ocular antihistamines bind to H1 receptors in the conjunctiva and this reduces itching but does not reduce redness.

Topical antihistamines provide faster and greater relief when compared to systemic antihistamines and are safe for pediatric patients(24). However, topical antihistamines do not have a long duration of action. Adverse reactions can include burning and stinging on instillation, headache, and dry mouth.

Levocabastine 0.05% suspension (Livostin®) and emedastine 0.05% solution (Emadine®) work primarily on H1 receptors. Emedastine is better at controlling itch and redness than levocabastine.(46,47) Emedastine is also superior to ketorolac (48), nedocromil (49), and oral loratadine (50) for reducing ocular itching and redness.

The effectiveness of levocabastine is similar to lodoxamide (51), which is a mast cell stabilizing agent, but it is less effective than ketorolac (41), a non-steroidal anti-inflammatory agent (NSAID).

An antihistamine/vasoconstrictor drug combination has been shown to be more effective than either agent alone.(41) In one study of 83 subjects, the combination of pheniramine and naphazoline was shown to be more effective than olopatadine (Patanol®) in alleviating allergy symptoms.(43) However, the short duration of action (less than 2 hours) limits the value of these medications.(24)

Mast cell stabilizers were originally approved for treatment of chronic allergic conditions such as GPC, AKC and VKC, but they have also been found to be effective for treatment of SAC and PAC.

Mast cell stabilizers work by inhibiting mast cell degranulation thereby reducing the release of inflammatory substances. However, these agents do not eliminate inflammatory mediators that have released prior to drug instillation. Therefore, mast cell stabilizers require a loading period of up to 2 weeks in order to achieve maximal efficacy.(24,52)

When long-term treatment is warranted, use of mast cell stabilizers should be considered. These drugs can provide an alternative to the use of topical steroids for the treatment of chronic allergic conjunctivitis.(16)

Cromolyn sodium 4% solution (Crolom®) was the first mast cell stabilizer to be developed and marketed for commercial use. Lodoxamide 0.1% solution (Alomide®), pemirolast 0.1% solution (Alamast®), and nedocromil 2% solution (Alocril®) are newer, more effective mast cell stabilizers.

Lodoxamide has been shown to produce more improvement in epithelial defects than cromolyn sodium in conditions such as VKC and AKC.(41) Pemirolast was also found to be more comfortable following instillation than nedocromil.(53) The low incidence of side-effects with these medications aids in ensuring patient compliance.(54)

Multiple-acting agents eliminate the need for prescribing two or more separate medications. These agents are typically fast-acting (onset less than 15 minutes) due to their antihistamine activity and have a prolonged duration of action (greater than 8 to12 hours) due to their mast cell stabilizing properties. This prolonged duration of action allows twice daily dosing. Contact lens wearers can instill one drop before contact lens insertion and another after contact lens removal. Multiple-acting agents have been shown to be safe for children over 3 years of age.(24,40)

Olopatadine 0.1% solution (Patanol®), ketotifen 0.025% solution (Zaditor®), azelastine 0.05% solution (Optivar®), and epinastine 0.05% solution (Elestat®) have both mast-cell stabilizing effects and antihistamine properties. These agents also inhibit other inflammatory mediators.

Olopatadine is effective in relieving signs and symptoms of chronic allergic conjunctivitis and can decrease the amount of mucus discharge.(18,62) Nearly 78% of patients with chronic allergies, such as VKC, AKC, and GPC, experienced relief as a result of taking olopatadine.(63)

Olopatadine has been shown to be superior to levocabastine (55), nedocromil (52), ketorolac (56), and oral loratadine (57) for relief of ocular itch. The use of olopatadine also allows greater comfort and longer duration of contact lens wear in patients who are experiencing allergy symptoms.(58) Studies are conflicting as to whether ketotifen and epinastine are more or less effective than olopatadine for allergy relief.(26,59,60,61)

NSAIDs inhibit prostaglandin production from arachidonic acid by blocking cyclooxygenase. In turn, this relieves itching and hyperemia. NSAIDs do not block other inflammatory mediators, such as histamine.(64)

Ketorolac 0.5% solution (Acular®) is currently the only NSAID approved for the treatment of ocular allergies, and it is not as effective as olopatadine or emedastine.(48,56) Up to 40% of patients experience stinging and burning with the use of ketorolac.(40)

Corticosteroids inhibit almost all inflammatory mediators. They block the synthesis of new histamine release by mast cells, inactivate available histamine, inhibit mast cell degranulation, decrease capillary permeability, and inhibit phospholipase A synthesis, which is used in the production of arachidonic acid.(64)

Topical steroids are often required to treat severe forms of allergic conjunctivitis, such as AKC, VKC, and GPC, in the acute phases of these diseases. Once the condition is controlled, the steroid should be tapered and treatment with mast cell stabilizers and antihistamines should be used. In the presence of a corneal ulcer, steroids can reduce the inflammation that is caused by the offending toxic substances.(65)

Patients using steroids, especially for long-term use, should be monitored due to the potential for side-effects, including increased intraocular pressure (IOP), formation of posterior subcapsular cataracts, and increased susceptibility to ocular infection. Steroid use should be limited due to these potential side-effects. Long-term treatment of VKC with topical steroids is responsible for induced glaucoma in 2% of patients.(15) If long-term use is required, rimexolone, fluorometholone, or loteprednol should be used because they are less likely to cause changes in IOP.

Loteprednol 0.2% suspension (Alrex®) is currently the only topical steroid approved for the relief of SAC signs and symptoms in the United States; it has also been found to be safe and effective for treating PAC.(64)

Loteprednol is rapidly metabolized upon instillation minimizing penetration into the anterior chamber. Of 343 patients taking loteprednol 0.2% for at least one year, none was found to have developed or experienced worsening of lenticular opacities. Although 20 patients developed a statistically significant rise in IOP, none had a clinically significant pressure increase.(64)

More potent topical steroids such as rimexolone 1% suspension (Vexol®), fluorometholone 0.1% suspension (FML®, Flarex®), loteprednol 0.5% suspension (Lotemax®), and prednisolone acetate 1% suspension (Pred Forte®) are not typically used as first-line treatment for SAC or PAC. These agents should be considered in severe cases and when other agents have been found to be ineffective.

Treatment failures due to poor patient compliance associated with drug costs can actually increase patient expense due to the need for more doctor visits, the necessity to try new medications, and the possibility of increased days of missed work.

Compliance can also be reduced due to ocular irritation upon instillation and excess tearing caused by drug preservatives required in multi-use bottles to reduce contamination and control microorganism growth. Excessive tearing can dilute the medication thus reducing its effectiveness and may require switching to a different medication or a non-preserved drug if one is available.

Instillation of most topical anti-allergy medications will be more comfortable, and the drops will provide addition relief, if the drugs are refrigerated and applied cold.(40)

Viscous drug preparations can increase contact time and therapeutic effect, but can also cause blurred vision.

Patients taking multiple topical medications should wait at least 5 minutes between drop instillations to prevent diluting the medications.

Short-term treatment with medications can relieve allergy symptoms such as itching and redness quickly, but long-term therapy is often necessary to prevent recurrences and to treat papillae and corneal complications. The need for long-term care can make treating ocular allergies expensive for the patient (or the patient's insurance company).

Approximate costs of topical medications commonly used for allergy management are shown in Table 1. Costs are approximate because of differences between pharmacies, variations in the number of drops per bottle, and the recommended dosages.(39)

Ikeda, et al., (39) found that the number of drops in a 5 ml bottle ranged from 100 to 170 and that one 5 ml bottle lasted between 12 and 52 days depending on patient usage. Accidentally missing the eye during application or accidentally instilling multiple drops will also increase medication cost.

In addition to topical and systemic medications, additional treatments can be beneficial for the management of chronic conditions such as VKC, AKC, and GPC.

Vernal keratoconjunctivitis

VKC should be treated aggressively in order to avoid corneal complications and permanent vision loss. Treatment should begin early in the spring and can be continued year-round if necessary. First-line treatment typically consists of topical anti-allergy medications such as mast cell stabilizers and antihistamines.

Systemic antihistamines and acetyl salicylic acid (aspirin 0.5 to 1.0 gram per day) can be considered if symptoms are still present following the use of topical anti-allergy medications.

A brief course (e.g., 3 to 5 days) of topical steroids might be necessary in severe cases.(15) The steroids are tapered over a one to two week period.

Abundant use of artificial tears will help to lubricate the eye and relieve any dryness.

Mucolytic agents, such as acetylcysteine, can be useful in the treatment of VKC. These agents aid in the removal of mucus discharge.

A topical, broad-spectrum, prophylactic antibiotic should be instilled in the presence of significant corneal involvement. Corneal complications associated with VKC should be monitored carefully and therapy adjusted as necessary, especially if steroids are being used. Follow-up examinations should be scheduled every 1 to 2 weeks during the acute phase and at least twice yearly during remissions.

Atopic keratoconjunctivitis

The goal of AKC treatment is to alleviate symptoms and preserve vision. Management of AKC consists mainly of topical mast cell stabilizers, steroids, and immunosuppressant medications. A topical, broad-spectrum, prophylactic antibiotic should also be instilled to prevent secondary infection if there is significant corneal involvement.

Other manifestations of atopic disease should be addressed during the treatment of AKC patients. Recommended therapies might including lid hygiene and antibiotic treatment to improve blepharitis and meibomian gland dysfunction.

Similar to the follow-up plan for VKC, any corneal complications should be monitored carefully and the therapy adjusted as necessary. Follow-up examinations should be scheduled every 1 to 2 weeks in the acute phase and at least twice yearly during remissions. In severe cases, hospitalization might be necessary to stabilize the condition.

Giant papillary conjunctivitis

Treatment of GPC includes improved contact lens hygiene, the use of disposable contact lenses, and/or modifying the contact lens design. Mast cell stabilizers and topical steroids have been shown to be effective in the treatment of GPC, but long-term use of steroids is not recommended due to the risk of potential side-effects.(5)

Refitting GPC patients with a different contact lens material has been shown to allow more than 80% of patients to wear lenses without further GPC symptoms.(37) Providing patients with a more frequent replacement schedule can also help. This approach has allowed 91% of patients to continue wearing contacts symptom-free.(37)

Wearing contact lenses for three weeks or less before replacement significantly decreases the incidence of GPC as compared to wearing them four weeks or longer.(37)

Redness, itching, and discharge will subside quickly following GPC treatment, but the papillae will take a longer time to subside.

Contact lens wear should be discouraged in severe or recurring cases of GPC.

The following cases illustrate the diagnosis and management of patients with SAC and VKC.

Case 1

A 37 year-old white female presented for a routine vision examination. She was wearing her last pair of contact lenses (CIBA Vision O₂Optix®, minus 1.75 D, 8.6 mm, 14.2 mm OU) and reported that she was happy with her vision using the lenses. The lenses were comfortable most of the year, but, for the last month, the right lens had become “goopy” after only one week of wear. She did not sleep in the lenses and cleaned them daily with Opti-Free RepleniSH®. The patient also reported that both eyes had been itchy for the last month and that she had to concentrate to not rub her eyes. She had experienced no sneezing or rhinitis and was taking over-the-counter Claritin® daily, which partially relieved the ocular itch.

Distance and near visual acuities with the contact lenses in place were 20/30 (6/9) OD and 20/20 (6/6) OS. Slit lamp examination of the 1-week-old lenses revealed 3+ lipid and protein deposits OD and trace deposits OS. The lenses were well centered and moved adequately with blinks.

After removal of the lenses, a refraction indicated that no change in the prescription was necessary. Slit lamp examination revealed grade 1 hyperemia OU. The cornea was clear with no sodium fluorescein staining, but there was trace papillae on the upper palpebral conjunctiva OU. The fundus examination of both eyes was unremarkable.

The patient was given new O₂Optix contact lenses. Because topical medications are more efficacious than systemic medications, she was instructed to discontinue the Claritin and begin Patanol® one drop in each eye following lens insertion in the morning and after lens removal at night. She was instructed to return for a follow-up examination in two weeks.

At her two-week follow-up, the patient reported that she had been using the Patanol® twice daily. Her lenses were comfortable throughout the day, and her eyes were not itching. Visual acuities were 20/20 (6/6) OD and OS, and the two-week-old contact lenses had no deposits. The patient was instructed to continue the Patanol® twice daily for the duration of the allergy season.

Case 2

An 8 year-old Hispanic male presented with a three week history of itchy, red eyes. The nasal area itched most, and the patient's mother reported that he was rubbing his eyes a lot. The itching worsened when he was when bathing, walking, or playing outdoors. The patient also reported a white stringy discharge as well as a stuffy nose, which began about the same time as the itchy eyes.

The mother was also concerned about the appearance of a white ring around the peripheral cornea.

The patient was taking no medications and had no history of medical allergies. He had been treated for itching at another clinic two week earlier, and was told to use cold compresses. However, these compresses did not provide sufficient relief.

Visual acuities were 20/20 (6/6) OD and OS. Slit lamp examination revealed grade 2 hyperemia OD and grade 1 hyperemia OS. The cornea showed grade 1 punctate epithelial defects (PEDs) that stained with sodium fluorescein. They were located inferiorly and surrounding the limbal area OU. Limbal papillae were present OU, and grade 2 papillae were visible on the superior palpebral conjunctiva OU.

The patient was diagnosed with vernal keratoconjunctivitis. Due to its known efficacy in the treatment of VKC and its safety profile with pediatric patients, Patanol® was prescribed to be used twice daily. The importance of using the medication on a regular basis was stressed to get the maximum mast cell stabilization effect. He was instructed to return for a follow-up examination in two weeks.

At the two week follow-up, the patient reported significantly decreased itching after using the Patanol® twice daily as prescribed. Visual acuities remained 20/20 (6/6) OD and OS. Slit lamp examination revealed trace hyperemia OU. The corneas had trace punctate epithelial defects, which stained with sodium fluorescein. They were located around the limbal areas of both eyes. Limbal papillae were still present OU, and grade 2 papillae were visible on the superior palpebral conjunctiva OU.

The patient was told to continue the Patanol® twice daily. Due to the risk of significant ocular problems, he will be evaluated every two weeks throughout the allergy season.

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Contact this Author:

Denise Goodwin, OD
Pacific University College of Optometry
2043 College Way
Forest Grove OR 97116

goodwin@pacificu.edu

Pacific University College of Optometry provides On-Line CE courses as a service to optometrists. The college does not endorse or recommend any products, equipment, or services that might be discussed in the courses. Courses are prepared by individuals believed to be experts in their areas of specialization who are compensated for their efforts. The College relies on their expertise to produce accurate and timely courses. Questions or concerns about courses should be directed to the individual authors and/or the Continuing Education Department at the College of Optometry at kundart@pacificu.edu.

Therapeutic Category	Available Agents	Recommended Dosage	Approximate Cost
Antihistamine/ vasoconstrictor	Antazoline/naphazoline (Vasocon-A®)	2 to 4 times daily	$7 for 15 mL; $10.50 for 30 ml
Antihistamine/ vasoconstrictor	Pheniramine/naphazoline (Opcon-A®, Naphcon-A®, Visine-A®)	2 to 4 times daily	$7 for 15 mL; $10.50 for 30 ml
Antihistamine	Levocabastine 0.05% suspension (Livostin®)	qid	$67 for 5 ml; $95 for 10 ml
Antihistamine	Emedastine 0.05% solution (Emadine®)	qid	$83 for 5 ml
Mast-cell Stabilizer	Cromolyn sodium 4% solution (Crolom®, Opticrom®)	4 to 6 times daily	$53 for (Crolom®); $62 for (Opticrom®); $39 for generic;10 ml
Mast-cell Stabilizer	Lodoxamide 0.1% solution (Alomide®)	qid	$104 for 10 ml
Mast-cell Stabilizer	Pemirolast 0.1% solution (Alamast®)	qid	$86 for 10 ml
Mast-cell Stabilizer	Nedocromil 2% solution (Alocril®)	bid	$99 for 5 ml
Multiple-acting Agent	Olopatadine 0.1% solution (Patanol®)	bid	$100 for 5 ml
Multiple-acting Agent	Ketotifen 0.025% solution (Zaditor®)	bid	$86 for 5 ml
Multiple-acting Agent	Azelastine 0.05% solution (Optivar®)	bid	$106 for 6 ml
Multiple-acting Agent	Epinastine 0.05% solution (Elestat®)	bid	$100 for 5 ml
Nonsteroidal Anti-Inflammatory Drugs	Ketorolac 0.5% solution (Acular®)	qid	$99 for 5 ml; $174 for 10 ml
Corticosteroids	Loteprednol 0.2% suspension (Alrex®)	qid	$68 for 5 ml; $125 for 10 ml

Drug	Preparation	Adult dosage
Cetirizine (Zyrtec®)	5 and 10 mg tablets 1 mg/ml syrup 5 and 10 mg chewable tablets	10 mg qd
Fexofenadine (Allegra®)	30, 60, and 180 mg tablets	60 mg bid or 180 mg qd
Loratadine (Claritin OTC®)	10 mg tablets 1 mg/ml syrup	10 mg qd
Desloratadine (Clarinex®)	5 mg tablets	5 mg qd

MANAGEMENT OF OCULAR ALLERGIES