Corneal anesthesia usually starts occurring within 15 seconds and lasts about 15 minutes. The blink reflex is temporarily lost, therefore the corneal epithelium may become dry. Protecting the eye from irritating chemicals, foreign bodies, and corneal scratches is important. The patient must be instructed that the affected eye will be insensitive to touch and to not rub, touch, or wipe the affected eye. Contact lenses may be reinserted after the anesthetic has completely worn off, usually after 20 minutes.

Before administering ophthalmic antiinfectives, the nurse should screen the patient for previous allergic reactions. Noninfectious conjunctivitis and local skin and eye irritation are possible side effects of ophthalmic antiinfective drugs.

Inflammation associated with keratoconjunctivitis sicca, causing lymphocytes to damage the lacrimal gland, results in fibrosis and loss of tear production; this can lead to xerophthalmia (dry eyes). Immunomodulators, such as cyclosporine ophthalmic emulsion, is an immunosuppressant that relieves xerophthalmia by a mechanism that is different from over-the-counter (OTC) lubricants. Ophthalmic cyclosporine acts as a partial immunomodulatory that causes apoptosis of lymphocytes and allows tear production to resume.

Ophthalmic nonsteroidal antiinflammatory drugs (NSAIDs) such as diclofenac sodium and ketorolac tromethamine inhibit miosis by preventing the formation of ocular prostaglandins. Most of these drugs are used for management or prevention of ocular inflammation before and following eye surgery. Unlike corticosteroids, NSAIDs do not affect intraocular pressure (IOP) (IOP is further discussed in Glaucoma and Ocular Hypertension Drugs). However, ocular NSAIDs can increase bleeding tendencies and delay corneal healing. Topical NSAIDs are not expected to increase cardiovascular risk, hepatic reactions, or other systemic adverse effects; however, ocular NSAIDs can cause bleeding of ocular tissues.

Ophthalmic corticosteroids such as dexamethasone and prednisolone acetate are another type of antiinflammatory. Corticosteroids are used to treat a number of eye conditions, such as allergic conjunctivitis, herpes zoster keratitis (not herpes simplex keratitis), corneal abrasion, postoperative ocular inflammation, and optic neuritis. Ocular corticosteroids can mask infections and delay healing and are contraindicated in persons with untreated ocular infections. Corticosteroids can worsen glaucoma by reducing the outflow of aqueous humor and increasing IOP; the effects are usually reversible upon discontinuation of the drug. Prolonged use can cause open-angle glaucoma, ocular nerve damage, or visual defects. Refer to Chapter 24 for more information on corticosteroids.

When allergies are the cause of eye inflammation, ophthalmic allergy drugs are commonly prescribed to treat the underlying cause. These allergy drugs contain antihistamines and mast cell stabilizers. Antihistamines block histamine from activating histamine receptors in the tissues. Degranulation of mast cells releases histamine and other inflammatory mediators; mast cell stabilizers prevent mast cells from degranulating. Ocular sensations that include burning, stinging, and blurred vision are common adverse effects reported. Other adverse effects include cephalgia, dysgeusia, and rhinitis.

Many brands and forms of ocular lubricants (artificial tears) are available OTC without a prescription. Although these agents are typically safe, the nurse must be alert to potential allergic reactions to preservatives found in lubricants.

There are two types of glaucoma, open-angle and angle-closure. In open-angle glaucoma, the trabecular network is open but becomes clogged (see Fig. 44.1B). Over time, as blockage of the trabecular network worsens, the IOP gradually increases, which damages the optic nerve.

In angle-closure glaucoma, also known as closed-angle or narrow-angle glaucoma, the iris is situated close to the drainage angle blocking the trabecular network (see Fig. 44.1C). Because the excess aqueous humor cannot drain, it builds up within the eye and increases IOP. When the drainage angle is completely blocked, eye pressure increases quickly, and the vision becomes suddenly blurred; this is a medical emergency and must be treated immediately. Management of angle-closure glaucoma is often surgical; however, pharmacologic management is sometimes indicated. Anticholinergic drugs (see Chapter 16) can cause mydriasis and can worsen angle-closure glaucoma.

Glaucoma is further classified as either primary or secondary. Primary glaucoma occurs because of a pathologic change within the eye that happens without a known cause. Primary open-angle glaucoma (POAG), the most common type of glaucoma, is a chronic condition that develops slowly over time as the trabecular meshwork becomes clogged for unknown reasons. Secondary glaucoma occurs in response to a known cause such as injury, disease, or medication. Although a number of drugs can increase the risk of secondary glaucoma, those that cause pupillary dilation are particularly problematic because they give the iris more flexibility to move toward the drainage angle, blocking the trabecular meshwork. People who are at risk for glaucoma should avoid decongestants. Certain herbal preparations (e.g., goldenseal, ephedra, and bitter orange) can also create problems when given to patients who have glaucoma.

Drugs for glaucoma (Table 44.4) belong to one of six drug categories: (1) prostaglandin analogues, (2) beta-adrenergic blockers, (3) alpha-adrenergic agonists, (4) cholinergic agents, (5) carbonic anhydrase inhibitors, or (6) systemic hyperosmotic drugs. Prostaglandin analogues and beta-adrenergic blockers are typically first-line therapy, followed by alpha-adrenergic agonists. Each category acts in different ways to decrease IOP. Even though damage due to glaucoma cannot be reversed, treatments may prevent further damage.