eMedicine Specialties > Ophthalmology > Conjunctiva

Conjunctivitis, Allergic: Treatment & Medication

Author: Parag A Majmudar, MD, Fellowship Co-Director, Department of Ophthalmology, Cornea and Refractive Surgery Service, Assistant Professor, Rush-Presbyterian-St Luke's Medical Center
Contributor Information and Disclosures

Updated: Oct 16, 2009

Treatment

Medical Care

• Seasonal and perennial allergic conjunctivitis
  • Pharmacologic intervention may 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.
  • Systemic and/or topical antihistamines may be given 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 affects, 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.
  • 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. 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). 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 one of the most potent pharmacologic agents used in the treatment of 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.
  • Corticosteroids exist in various forms and potencies. Relatively weak steroids, such as rimexolone, medrysone, and fluorometholone, tend to have less potency 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%), a steroid, 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. Alrex has a specific indication for ocular allergy and has been shown in clinical studies to have fewer ocular adverse effects. However, a general rule-of-thumb is that topical steroids should be prescribed only for a short period of time and for severe cases that do not respond to conventional therapy.
• Vernal keratoconjunctivitis
  • Various 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. Similarly, topical antihistamines have no significant long-term benefit.
  • Mast cell stabilizers 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. Pulsed-therapy regimen is generally recommended, such as 1% prednisolone acetate 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) may be effective in reducing some of the signs and symptoms of VKC without adverse effects. Oral aspirin has been shown to be effective. Treatment of corneal shield ulcer may require antibiotic-steroid ointments.
• Atopic keratoconjunctivitis
  • Treatment of patients with AKC is similar to that of VKC, in that it includes controlling the environment and avoiding allergens and may require topical and systemic medications to provide symptomatic relief. As with VKC, topical vasoconstrictors and antihistamines may provide very limited, short-term relief; they are not the mainstay of treatment.
  • As with VKC, topical mast cell stabilizers and topical corticosteroids provide significant relief of symptoms. Mast cell stabilizers have to be used for several weeks prior to seeing a clinical effect, and, 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 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.³
• Giant papillary conjunctivitis
  • Goal of treatment in GPC is resolution of symptoms and restoration of functional use of contact lenses or ocular prosthetics. Although removal of the responsible foreign body is the definitive treatment, and while 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 a patient 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 because of 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 similar to that in the other immunologic conjunctival disorders discussed previously. As always, care must be taken when using topical corticosteroids; pulsed regimen is recommended to minimize adverse reactions.

Surgical Care

• Vernal keratoconjunctivitis
  • 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.
• Atopic keratoconjunctivitis: Penetrating keratoplasty may be undertaken in cases of severe corneal scarring or thinning, but great attention to control ocular surface inflammation is required.

Consultations

Allergists may help in identifying the responsible allergen(s).

Medication

Topical antihistamines

Act by competitive inhibition of histamine at the H1 receptor. Block effects of endogenously released histamine.

Emedastine difumarate (Emadine)

Relatively selective H-receptor antagonist for topical administration. The 0.05% ophthalmic solution contains 0.884 mg/mL of emedastine difumarate.

Levocabastine (Livostin)

Selective histamine H1 receptor antagonist. Active ingredient is 0.54 mg levocabastine hydrochloride.

Epinastine (Elestat)

Direct histamine-1 receptor antagonist. Does not penetrate blood-brain barrier and therefore should not induce adverse CNS effects. Indicated for symptoms due to allergic conjunctivitis.

Azelastine (Optivar)

Competes with H1-receptor sites on effector cells and inhibits release of histamine and other mediators involved in allergic response.

Bepotastine besilate ophthalmic solution (Bepreve)

Topically active antihistamine that directly antagonizes H1-receptors and inhibits release of histamine from mast cells. Indicated for itching associated with allergic conjunctivitis.

Mast cell stabilizers

Inhibit sensitized mast cell degeneration when exposed to specific antigens by inhibiting the release of mediators from the mast cells. Block calcium ions from entering the mast cell.

Lodoxamide tromethamine (Alomide)

Mast cell stabilizer. Active ingredient is 1.78 mg lodoxamide tromethamine.

Olopatadine (Patanol, Pataday)

Relatively selective H1 receptor antagonist and inhibitor of histamine release from mast cell. Active ingredient of Patanol is 1.11 mg olopatadine hydrochloride; Pataday is 2.22 mg olopatadine hydrochloride.

Ketotifen (Zaditor)

Over-the-counter (OTC) antihistamine eye drop. Noncompetitive H1-receptor antagonist and mast cell stabilizer. Inhibits release of mediators from cells involved in hypersensitivity reactions.

Nedocromil (Alocril)

Interferes with mast cell degranulation, specifically with release of leukotrienes and platelet activating factor.

Corticosteroids

Have both anti-inflammatory (glucocorticoid) and salt retaining (mineralocorticoid) properties. Glucocorticoids have profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.

Loteprednol etabonate (Lotemax, Alrex)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. Topical ester steroid drop with decreased risk of glaucoma. Available in 0.2% and 0.5% drops.

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Their mechanism of action is believed to be through inhibition of the cyclooxygenase enzyme that is essential in the biosynthesis of prostaglandins, which results in vasoconstriction, decrease in vascular permeability and leukocytosis, and a decrease on intraocular pressure.

Ketorolac tromethamine (Acular)

Pyrrolo-pyrrole group of NSAIDs. Inhibits prostaglandin synthesis by decreasing activity of the enzyme, cyclooxygenase, which results in decreased formation of prostaglandin precursors, which, in turn, results in reduced inflammation. Active ingredient is 0.5% ketorolac tromethamine.

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