Glaucoma

Glaucoma

Glaucoma is a group of ocular conditions characterized by optic nerve damage. The optic nerve damage is related to the IOP caused by congestion of aqueous humor in the eye. There is a range of pressures that have been considered “normal” but that may be associated with vision loss in some patients. Glaucoma is one of the leading causes of irreversible blindness in the world and is the leading cause of blindness among adults in the United States. It is estimated that at least 2 million Americans have glau-coma and that 5 to 10 million more are at risk (Margolis et al., 2002). Glaucoma is more prevalent among people older than 40 years of age, and the incidence increases with age. It is also more prevalent among men than women and in the African American and Asian populations (Chart 58-3). There is no cure for glaucoma, but research continues.

Aqueous Humor and Intraocular Pressure

Aqueous humor flows between the iris and the lens, nourishing the cornea and lens. Most (90%) of the fluid then flows out of the anterior chamber, draining through the spongy trabecular meshwork into the canal of Schlemm and the episcleral veins (Fig. 58-7). About 10% of the aqueous fluid exits through the cil-iary body into the suprachoroidal space and then drains into the venous circulation of the ciliary body, choroid, and sclera. Unim-peded outflow of aqueous fluid depends on an intact drainage sys-tem and an open angle (about 45 degrees) between the iris and the cornea. A narrower angle places the iris closer to the trabecu-lar meshwork, diminishing the angle. The amount of aqueous humor produced tends to decrease with age, in systemic diseases such as diabetes, and in ocular inflammatory conditions.

IOP is determined by the rate of aqueous production, the re-sistance encountered by the aqueous humor as it flows out of the passages, and the venous pressure of the episcleral veins that drain into the anterior ciliary vein. When aqueous fluid production and drainage are in balance, the IOP is between 10 and 21 mm Hg. When aqueous fluid is inhibited from flowing out, pressure builds up within the eye. Fluctuations in IOP occur with time of day, exertion, diet, and medications. It tends to increase with blinking, tight lid squeezing, and upward gazing. Systemic con-ditions such as hypertension and intraocular conditions such as uveitis and retinal detachment have been associated with elevated IOP. Exposure to cold weather, alcohol, a fat-free diet, heroin, and marijuana have been found to lower IOP.

Pathophysiology

There are two accepted theories regarding how increased IOP damages the optic nerve in glaucoma. The direct mechanical the-ory suggests that high IOP damages the retinal layer as it passes through the optic nerve head. The indirect ischemic theory sug-gests that high IOP compresses the microcirculation in the optic nerve head, resulting in cell injury and death. Some glaucomas appear as exclusively mechanical, and some are exclusively is-chemic types. Typically, most cases are a combination of both.

Regardless of the cause of damage, glaucomatous changes typ-ically evolve through clearly discernible stages:

Initiating events: precipitating factors include illness, emo-tional stress, congenital narrow angles, long-term use of corticosteroids, and mydriatics (ie, medications causing pupillary dilation). These events lead to the second stage.

Structural alterations in the aqueous outflow system: tissueand cellular changes caused by factors that affect aqueous humor dynamics lead to structural alterations and to the third stage.

Functional alterations: conditions such as increased IOP orimpaired blood flow create functional changes that lead to the fourth stage.

Optic nerve damage: atrophy of the optic nerve is charac-terized by loss of nerve fibers and blood supply, and this fourth stage inevitably progresses to the fifth stage.

Visual loss: progressive loss of vision is characterized byvisual field defects.

Classification of Glaucoma

There are several types of glaucoma. Whether glaucoma is known as open-angle or angle-closure glaucoma depends on which mech-anisms cause impaired aqueous outflow. Glaucoma can be primary or secondary, depending on whether associated factors con-tribute to the rise in IOP.

Although glaucoma classification is changing as knowledge in-creases, current clinical forms of glaucoma are open-angle glau-comas, angle-closure glaucomas (also called pupillary block), congenital glaucomas, and glaucomas associated with other con-ditions, such as developmental anomalies, corticosteroid use, and other ocular conditions. The two common clinical forms of glau-coma encountered in adults are open-angle and angle-closure glaucoma. Table 58-4 explains the general characteristics of the different types of open-angle and angle-closure glaucomas.

Clinical Manifestations

Glaucoma is often called the silent thief of sight because most pa-tients are unaware that they have the disease until they have ex-perienced visual changes and vision loss. The patient may not seek health care until he or she experiences blurred vision or “halos” around lights, difficulty focusing, difficulty adjusting eyes in low lighting, loss of peripheral vision, aching or discomfort around the eyes, and headache.

Assessment and Diagnostic Findings

The purpose of a glaucoma workup is to establish the diagnostic category, assess the optic nerve damage, and formulate a treat-ment plan. The patient’s ocular and medical history must be de-tailed to investigate the history of predisposing factors. There are four major types of examinations used in glaucoma evaluation, diagnosis, and management: tonometry to measure the IOP, ophthalmoscopy to inspect the optic nerve, gonioscopy to exam-ine the filtration angle of the anterior chamber, and perimetry to assess the visual fields.

The changes in the optic nerve significant for the diagnosis of glaucoma are pallor and cupping of the optic nerve disc. The pal-lor of the optic nerve is caused by a lack of blood supply that re-sults from cellular destruction. Cupping is characterized by exaggerated bending of the blood vessels as they cross the optic disc, resulting in an enlarged optic cup that appears more basin-like compared with a normal cup. The progression of cupping in glaucoma is caused by the gradual loss of retinal nerve fibers ac-companied by the loss of blood supply, resulting in increased pal-lor of the optic disc.

As the optic nerve damage increases, visual perception in the area is lost. The localized areas of visual loss (ie, scotomas) represent loss of retinal sensitivity and are measured and mapped by perime-try. The results are mapped on a graph. In patients with glaucoma, the graph has a distinct pattern that is different from other ocular diseases and is useful in establishing the diagnosis. Figure 58-8 shows the progression of visual field defects caused by glaucoma.

Medical Management

The aim of all glaucoma treatment is prevention of optic nerve damage through medical therapy, laser or nonlaser surgery, or a combination of these approaches. Lifelong therapy is almost al-ways necessary because glaucoma cannot be cured. Although treatment cannot reverse optic nerve damage, further damage can be controlled. The treatment goal is to maintain an IOP within a range unlikely to cause further damage.

The initial target for IOP among patients with elevated IOP and those with low-tension glaucoma with progressive visual field loss is typically set at 30% lower than the current pressure. The patient is monitored for the stability of the optic nerve. If there is evidence of progressive damage, the target IOP is again lowered until the optic nerve shows stability.

Treatment focuses on achieving the greatest benefit at the least risk, cost, and inconvenience to the patient. All treatment options have potential complications, especially surgery, which yields the best success rates. In the United States, medical management is the common approach, and surgical management is the last re-sort. In Great Britain, the initial treatment of choice is surgery (Fechtner & Singh, 2001).

PHARMACOLOGIC THERAPY

Medical management of glaucoma relies on systemic and topical ocular medications that lower IOP. Periodic follow-up examina-tions are essential to monitor IOP, appearance of the optic nerve, visual fields, and side effects of medications. In considering a therapeutic regimen, the ophthalmologist aims for the greatest ef-fectiveness with the least side effects, inconvenience, and cost. Therapy takes into account the patient’s health and stage of glau-coma. Comfort, affordability, convenience, lifestyle, and person-ality are factors to consider in the patient’s compliance with the medical regimen.

The patient is usually started on the lowest dose of topical medication and then advanced to increased concentrations until the desired IOP level is reached and maintained. Because of their efficacy, minimal dosing (can be used once each day), and low cost, beta-blockers are the preferred initial topical medications. One eye is treated first, with the other eye used as a control in de-termining the efficacy of the medication; once efficacy has been established, treatment of the fellow eye is started. If the IOP is el-evated in both eyes, both are treated. When results are not satis-factory, a new medication is substituted. The main markers of the efficacy of the medication in glaucoma control are lowering of the IOP to the target pressure, appearance of the optic nerve head, and the visual field.

Several types of ocular medications are used to treat glaucoma (Table 58-5), including miotics (ie, cause pupillary constriction), adrenergic agonists (ie, sympathomimetic agents), beta-blockers, alpha₂-agonists (ie, adrenergic agents), carbonic anhydrase in-hibitors, and prostaglandins. Cholinergics (ie, miotics) increase the outflow of the aqueous humor by affecting ciliary muscle con-traction and pupil constriction, allowing flow through a larger opening between the iris and the trabecular meshwork. Adrener-gic agonists increase aqueous outflow but primarily decrease aqueous production with an action similar to beta-blockers and carbonic anhydrase inhibitors.

SURGICAL MANAGEMENT

In laser trabeculoplasty for glaucoma, laser burns are applied to the inner surface of the trabecular meshwork to open the intra-trabecular spaces and widen the canal of Schlemm, thereby promoting outflow of aqueous humor and decreasing IOP. 

The pro-cedure is indicated when IOP is inadequately controlled by med-ications; it is contraindicated when the trabecular meshwork cannot be fully visualized because of narrow angles. A serious complication of this procedure is a transient rise in IOP (usually 2 hours after surgery) that may become persistent. IOP assess-ment in the immediate postoperative period is essential.

In laser iridotomy for pupillary block glaucoma, an opening is made in the iris to eliminate the pupillary block. Laser iridotomy is contraindicated in patients with corneal edema, which inter-feres with laser targeting and strength. Potential complications are burns to the cornea, lens, or retina; transient elevated IOP; closure of the iridotomy; uveitis; and blurring. Pilocarpine is usu-ally prescribed to prevent closure of the iridotomy.

Filtering procedures for chronic glaucoma are used to create anopening or fistula in the trabecular meshwork to drain aqueous humor from the anterior chamber to the subconjunctival space into a bleb, thereby bypassing the usual drainage structures. This allows the aqueous humor to flow and exit by different routes (ie, absorption by the conjunctival vessels or mixing with tears). Trabeculectomy is the standard filtering technique used to removepart of the trabecular meshwork. Complications include hemor-rhage, an extremely low (hypotony) or elevated IOP, uveitis, cataracts, bleb failure, bleb leak, and endophthalmitis. Unlike other surgical procedures, the filtering procedure’s goal in glaucoma treatment is to achieve incomplete healing of the surgical wound. The outflow of aqueous humor in a newly created drain-age fistula is circumvented by the granulation of fibrovascular tissue or scar tissue formation on the surgical site. Scarring is in-hibited by using antifibrosis agents such as the antimetabolites fluorouracil (Efudex) and mitomycin (Mutamycin). Like all anti-neoplastic agents, they require special handling procedures before, during, and after the procedure. Fluorouracil can be administered intraoperatively and by subconjunctival injection during follow-up; mitomycin is much more potent and is administered only intraoperatively.

Drainage implants or shunts are open tubes implanted in theanterior chamber to shunt aqueous humor to an attached plate in the conjunctival space. A fibrous capsule develops around the episcleral plate and filters the aqueous humor, thereby regulating the outflow and controlling IOP.

Nursing Management

TEACHING PATIENTS ABOUT GLAUCOMA CARE

The medical and surgical management of glaucoma slows the progression of glaucoma but does not cure it. The lifelong thera-peutic regimen mandates patient education. The nature of the disease and the importance of strict adherence to the medication regimen must be explained to help ensure compliance. A thor ough patient interview is essential to determine systemic condi-tions, current systemic and ocular medications, family history, and problems with compliance to glaucoma medications. Then the medication program can be discussed, particularly the inter-actions of glaucoma-control medications with other medications. For example, the diuretic effect of acetazolamide has an additive effect on the diuretic effects of other antihypertensive medica-tions and can result in hypokalemia. The effects of glaucoma-control medications on vision must also be explained. Miotics and sympathomimetics result in altered focus; therefore, patients need to be cautious in navigating their surroundings. Informa-tion about instilling ocular medication and preventing systemic absorption with punctal occlusion is described in the section on ophthalmic medications.

Nurses in all settings encounter patients with glaucoma. Even patients with long-standing disease and those with glaucoma as a secondary diagnosis should be assessed for knowledge level and compliance with the therapeutic regimen. Chart 58-4 contains points to review with glaucoma patients.

CONTINUING GLAUCOMA CARE AT HOME

For patients with severe glaucoma and impaired function, refer-ral to services that assist the patient in performing customary ac-tivities may be needed. The loss of peripheral vision impairs mobility the most. These patients need to be referred to low-vision and rehabilitation services. Patients who meet the criteria for legal blindness should be offered referrals to agencies that assist in obtaining federal assistance.

Reassurance and emotional support are important aspects of care. A lifelong disease involving a possible loss of sight has psy-chological, physical, social, and vocational ramifications. 

The family must be integrated into the plan of care, and because the disease has a familial tendency, family members should be en-couraged to undergo examinations at least once every 2 years to detect glaucoma early.