Allergic Conjunctivitis Treatment & Management
- Author: Mark Ventocilla, OD, FAAO; Chief Editor: John D Sheppard, Jr, MD, MMSc more...
Avoidance of the offending antigen is the primary behavioral modification for all types of allergic conjunctivitis. In other respects, management of allergic conjunctivitis varies somewhat according to the specific subtype (SAC, PAC, GPC, VKC, AKC).
Allergic conjunctivitis can be treated with a variety of medications, including topical antihistamines, mast cell stabilizers, nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids. Surgical intervention may be indicated in severe cases of VKC or AKC.
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Management of Seasonal and Perennial Allergic Conjunctivitis
Pharmacologic intervention may be necessary to help alleviate the symptoms of acute allergic conjunctivitis. Various classes of medication may be effective against the symptoms of acute allergic conjunctivitis; each is directed at a specific point in the inflammatory and allergic cascade.
Artificial tear substitutes provide a barrier function and help to improve the first-line defense at the level of conjunctival mucosa. These agents help to dilute various allergens and inflammatory mediators that may be present on the ocular surface, and they help flush the ocular surface of these agents. Chilled tears, as well as any topical medication, provide an added degree of relief, as well as homeopathic vasoconstriction.
Systemic and/or topical antihistamines may be prescribed to relieve acute symptoms due to interaction of histamine at ocular H1 and H2 receptors. While systemic antihistamines often relieve ocular allergic symptoms, patients may experience systemic adverse effects, such as drowsiness and dry mouth.
Topical antihistamines competitively and reversibly block histamine receptors and relieve itching and redness but only for a short time. These medications do not affect other proinflammatory mediators, such as prostaglandins and leukotrienes, which remain uninhibited. A number of topical antihistamines are available, including epinastine (Elestat) and azelastine (Optivar). Both are potent antihistamines that have a rapid onset and are effective in relieving the signs and symptoms of allergic conjunctivitis.
Vasoconstrictors are available either alone or in conjunction with antihistamines to provide short-term relief of vascular injection and redness. Common vasoconstrictors include naphazoline, phenylephrine, oxymetazoline, and tetrahydrozoline. Generally, the common problem with vasoconstrictors is that they may cause rebound conjunctival injection and inflammation. These pharmacologic agents are ineffective against severe ocular allergies and against other more severe forms of allergic conjunctivitis, such as atopic and vernal disease. They can also produce dependency and progressive tachyphylaxis, thereby adding continuously increasing medication and preservative toxicity to the clinical picture.
Mast cell stabilizers
Mast cell stabilizers have a mechanism of action that is unclear. They may aid in the phosphorylation of a 78,000-d protein that terminates secretion of mast cell granules; they may increase calcium influx into the cell preventing membrane changes; and/or they may reduce membrane fluidity prior to mast cell degranulation. The end result is a decrease in degranulation of mast cells, which prevents release of histamine and other chemotactic factors that are present in the preformed and newly formed state.
Note that mast cell stabilizers do not relieve existing symptoms and are to be used on a prophylactic basis to prevent mast cell degranulation with subsequent exposure to the allergen. Therefore, they need to be used long term in conjunction with various other classes of medications. Common mast cell stabilizers include cromolyn sodium and lodoxamide (Alomide). Alcaftadine (Lastacaft), bepotastine (Bepreve), olopatadine (Patanol), nedocromil (Alocril), and ketotifen (Zaditor) are mast cell stabilizers and inhibit histamine release.
Nonsteroidal anti-inflammatory drugs (NSAIDs) act on the cyclooxygenase metabolic pathway and inhibit production of prostaglandins and thromboxanes. They have no role in blocking mediators formed by the lipoxygenase pathway, such as leukotrienes. Common NSAIDs that are approved for allergic indications include ketorolac tromethamine (Acular).
Corticosteroids remain among the most potent pharmacologic agents used in the treatment of chronic ocular allergy. They act at the first step of the arachidonic acid pathway by inhibiting phospholipase, which is responsible for converting membrane phospholipid into arachidonic acid. By preventing the formation of arachidonic acid, corticosteroids effectively block both cyclooxygenase and lipoxygenase pathways, in contrast to NSAIDs, which act only on the cyclooxygenase pathway.
Corticosteroids do have limitations, including ocular adverse effects, such as delayed wound healing, secondary infection, elevated intraocular pressure, and formation of cataract. In addition, the anti-inflammatory and immunosuppressive affects are nonspecific. As a rule, topical steroids should be prescribed only for a short period of time and for severe cases that do not respond to conventional therapy.
Corticosteroids exist in various forms and potencies. Relatively weak steroids, such as rimexolone, medrysone, and fluorometholone, tend to have less potency in the eye, with fewer ocular adverse effects. In contrast, agents such as prednisolone acetate are more potent and have a higher incidence of adverse effects.
Loteprednol etabonate (Lotemax 0.05% and Alrex 0.02%), is an ester steroid, which is rapidly metabolized once it enters the anterior chamber of the eye. Therefore, it is extremely useful in treating ocular surface and superficial corneal inflammations owing to its favorable safety profile and therapeutic index. Alrex has a specific indication for ocular allergy and has been shown in clinical studies to have fewer ocular adverse effects. Lotemax is indicated for SAC and GPC with concomitant contact lens use.
Immunotherapy is a mainstay in the systemic management of allergies. Traditionally, immunotherapy is delivered via subcutaneous injection. However, sublingual (oral) immunotherapy (SLIT) is gaining momentum among allergists. Numerous articles have analyzed the effects of SLIT on allergic conjunctivitis. Preliminary indications are that SLIT may have a moderate effect on the signs and symptoms of allergic conjunctivitis, but further analysis is necessary. A 2012 study confirmed that SLIT may significantly reduce symptoms in children with grass pollen–allergic rhinoconjunctivitis. The preparation studied had significant effects on allergen-specific antibodies and was well tolerated.
Management of Vernal Keratoconjunctivitis
Multiple pharmacologic agents may be used to provide varying degrees of relief. Mucolytic agents, such as acetylcysteine, may help minimize the discharge and provide temporary relief. Vasoconstrictors may reduce hyperemia but are not effective in severe cases on a long-term basis. Moreover, the long-term use of vasoconstrictors may have a rebound effect, leaving the eye untreatably injected. Similarly, topical antihistamines have no significant long-term benefit.
Mast cell stabilizers, with antihistamine effects, are perhaps the mainstay of treatment of VKC and are safe for long-term use. However, topical corticosteroids generally become necessary for most patients with significant symptoms. Because of their potential adverse effects, topical steroids should be prescribed at the lowest effective concentration and for the shortest duration possible.
A pulsed-therapy steroid regimen is generally recommended every 2 hours for the first week followed by a rapid taper; this may be repeated if symptoms recur. Systemic steroids may be used but generally are not necessary for moderate cases of VKC.
Several reports have shown that topical cyclosporine (Restasis), indicated for the use in keratoconjunctivitis sicca, may be effective in reducing some of the signs and symptoms of VKC without adverse effects. Oral aspirin has been shown to be effective in relieving some of the inflammation associated with allergy. Treatment of corneal shield ulcer may require antibiotic-steroid ointments.
A wide variety of steroid-sparing regimens have been used in the treatment of more severe ocular allergies such as AKC and VKC. These include substitution of ester steroids for the traditionally more side-effect–prone ketone steroids, as well as systemic medications including montelukast or methotrexate, or the numerous available oral antihistamines such as loratadine, fexofenadine, and cetirizine.
Severe cases of corneal shield ulcer may require superficial keratectomy to promote epithelial regeneration. Generally, shield ulcers are chronic conditions that are often refractory to conventional therapy. There have been reports of excimer laser phototherapeutic keratectomy (PTK) being used to remove fibrin deposits on the Bowman layer and theoretically facilitate epithelial healing.
Other surgical procedures, such as cryoablation of giant papillae or surgical removal of papillae with mucosal grafting, generally are not required, but they may be helpful in extremely advanced cases. Remember that since VKC is a self-limited disease, extensive reconstructive surgery may not have an acceptable risk-benefit ratio.
Management of Atopic Keratoconjunctivitis
Treatment of patients with AKC, similar to that for VKC, consists of controlling the environment and avoiding allergens. These patients may require topical and systemic medications to ultimately provide real symptomatic relief. As with VKC, topical vasoconstrictors and antihistamines may provide very limited, short-term relief; they are not the mainstay of treatment.
The use of topical mast cell stabilizers and topical corticosteroids provide significant relief of symptoms. Mast cell stabilizers have to be used for several weeks before taking effect; in the interim, topical steroids used in a pulsed fashion may help to control symptoms. Systemic antihistamines that are specific for H1 histamine receptors have been found to be helpful. Systemic steroids rarely are required, except in cases of vision-threatening complications.
Systemic cyclosporine, which has been shown to be effective in the treatment of atopic dermatitis, has also shown promise in controlling ocular inflammation in AKC. Postulated mechanism of action is inhibition of the ability of T lymphocytes to produce interleukin 2 (IL-2), which is responsible for recruiting and activating new T cells. However, as with any systemic therapy, adverse effects may be significant; therefore, monitoring of serum levels and renal function is essential.
Concomitant herpes simplex virus infection should be treated with either topical or oral antiviral agents as needed. A subset of patients with recalcitrant and debilitating AKC may benefit from plasmapheresis, as was described by Aswad in 2 patients, one of whom had hyperimmunoglobulinemia E.
Penetrating keratoplasty may be undertaken in cases of severe corneal scarring or thinning. However, great attention to control ocular surface inflammation is required.
Management of Giant Papillary Conjunctivitis
Resolution of symptoms and restoration of functional use of contacts lenses or ocular prosthetics are the main goals of treatment for GPC. Although removal of the responsible foreign body is the definitive treatment, and that may be appropriate for exposed sutures or scleral buckles, complete discontinuation of contact lenses or ocular prosthetics may be met with some degree of resistance from patients. Fortunately, contact lens wear does not need to be completely discontinued to minimize the symptoms of GPC.
Significant reduction in the signs and symptoms may be achieved by changing the contact lens care routine. Disinfecting solutions that contain chemical preservatives should be discontinued. Converting from soft daily-wear contact lenses to disposable or daily-disposable soft contact lenses may prevent the accumulation of proteinaceous deposits, which may be the antigenic stimulus for GPC.
Rigid gas-permeable contact lenses may provide further relief from symptoms if disposable lenses do not provide adequate response. This relief is due to the decreased proclivity of the rigid gas-permeable contact lenses to develop adherent deposits and coatings.
Pharmacologic treatment of GPC includes the use of mast cell stabilizers, topical corticosteroids, and antihistamines, in a manner similar to that in the other immunologic conjunctival disorders discussed previously. As always, care must be taken when using topical corticosteroids; a pulsed regimen is recommended to minimize adverse reactions. Loteprednol is ideally suited when long-term topical steroid therapy is indicated.
Prevention of Allergic Conjunctivitis
Seasonal and perennial allergic conjunctivitis
Avoidance of the offending antigen is the primary behavioral modification; specific testing by an allergist will identify the responsible allergen(s) and help the individual to establish ways to avoid the allergen. Contact reactions caused by medications or cosmetics are also treated best by avoidance.
As with most type I hypersensitivity disorders, allergen avoidance should be emphasized as the first-line treatment. Although permanent relocation to a cooler climate is not feasible in many cases, it remains a very effective therapy for VKC.
Maintenance of an air-conditioned environment and control of dust particles at home and work may also be beneficial. Local measures, such as cold compresses and periodic instillation of artificial tears, have also been shown to provide temporary relief.
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Wahn U, Klimek L, Ploszczuk A, Adelt T, Sandner B, Trebas-Pietras E, et al. High-dose sublingual immunotherapy with single-dose aqueous grass pollen extract in children is effective and safe: A double-blind, placebo-controlled study. J Allergy Clin Immunol. 2012 Aug 29. [Medline].
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Abelson MB, Gomes PJ, Vogelson CT, Pasquine TA, Turner FD, Wells DT, et al. Effects of a new formulation of olopatadine ophthalmic solution on nasal symptoms relative to placebo in two studies involving subjects with allergic conjunctivitis or rhinoconjunctivitis. Curr Med Res Opin. 2005 May. 21(5):683-91. [Medline].
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|Age at onset||Generally presents at a younger age than AKC' first decade||Second to third decade|
|Sex||Males are affected preferentially.||No sex predilection|
|Seasonal variation||Typically occurs during spring months||Generally perennial|
|Discharge||Thick mucoid discharge||Watery and clear discharge|
|Conjunctival scarring||Moderate incidence of conjunctival scarring||Higher incidence of conjunctival scarring|
|Horner-Trantas dots||Horner-Trantas dots and shield ulcers are commonly seen.||Presence of Horner-Trantas dots is rare.|
|Corneal neovascularization||Not present, unless secondary to infectious keratitis||Deep corneal neovascularization tends to develop|
|Presence of eosinophils in conjunctival scraping||Conjunctival scraping reveals eosinophils to a greater degree in VKC than in AKC||Presence of eosinophils is less likely|