Management of Glaucoma

Laura C. Fine

Claudia U. Richter

Glaucoma is a chronic, progressive optic neuropathy characterized by acquired atrophy of the optic nerve and loss of retinal ganglion cells and their axons. Elevated intraocular pressure (IOP) and other, less well-understood factors contribute to progressive optic nerve cupping and visual field loss. Glaucoma is one of the leading preventable causes of legal blindness in the United States. In managing the glaucoma patient, the ophthalmologist strives to achieve a stable range of IOPs deemed likely to retard further optic nerve damage and preserve vision.

Management poses a challenge for the patient and the doctor because glaucoma is chronic, is often asymptomatic, and requires daily use of eye medications, which may be costly and cause adverse side effects. When medications are ineffective or not tolerated, interventional measures such as laser and surgery need consideration. Substantial visual field loss in glaucoma is associated with a decrease in quality of life measures.

Although the primary physician is not responsible for the definitive diagnosis or treatment of glaucoma, it remains important to identify patients at risk (see Chapter 198) and recognize early stages of optic nerve damage. The primary physician should also be familiar with the systemic effects of topical and oral glaucoma medications and the potential interaction between certain systemic medications and glaucoma.

PATHOPHYSIOLOGY AND CLINICAL PRESENTATION (1, 2, 3, 4, 5, 6, 7 and 8)

Pathophysiology

The IOP is maintained by the dynamic equilibrium of aqueous production and outflow. The iris divides the anterior portion of the eye into anterior and posterior chambers, which communicate through the pupil. Aqueous humor, produced by the ciliary body, fills the posterior chamber, flows through the pupil into the anterior chamber, and leaves the eye through the trabecular meshwork, a connective tissue filter at the angle between the iris and the cornea. The aqueous passes through the trabecular meshwork into Schlemm’s canal and into the episcleral venous system.

Although elevated IOP is not part of the definition of glaucoma, IOP is the only modifiable risk factor. Increased IOP is caused by obstruction to outflow. In open-angle glaucoma (OAG), obstruction exists at a microscopic level in the trabecular meshwork. In angle-closure glaucoma (ACG), the iris obstructs the trabecular meshwork due to an anatomic variation causing pupillary block and obstruction of aqueous humor flow into the anterior chamber. Increased IOP increases vascular resistance, causing decreased vascular perfusion of the optic nerve and ischemia and direct damage to the axons in the optic nerve. The increased pressure interferes with axoplasmic flow in the ganglion cell axons, causing cell dysfunction and death, and it compresses the lamina cribrosa—the sievelike structure through which axons pass when leaving the eye. The altered supporting structure may then interfere with axonal function. These different mechanisms of axonal damage are of variable importance in different patients, but the final result is loss of ganglion cells and their axons, increased optic nerve cupping, and visual field loss.

Risk Factors and Clinical Presentation

Open-Angle Glaucoma

This form of glaucoma accounts for more than 90% of cases and has multiple risk factors (elevated ocular pressure, age >50 years, family history of glaucoma, African American or Hispanic race, thinner central cornea, myopia, type 2 diabetes, and use of oral, inhaled, or topical steroids). There appears to be a subset of patients with low ocular perfusion pressures (mean arterial blood pressure minus intraocular pressure) who are at higher risk for OAG. Population-based studies find that low diastolic pressure (<50 mm Hg) is associated with a higher prevalence of primary open-angle glaucoma (POAG). In addition, migraine headache and peripheral vasospasm have been identified as risk factors for glaucomatous optic nerve damage. The effect of concurrent cardiovascular disease and systemic hypertension on OAG has not been demonstrated consistently.

POAG represents a spectrum of disease, in which the susceptibility of the optic nerve to damage varies among patients. While many POAG patients present with elevated IOP, other patients may not have elevated IOP measurements but still demonstrate the characteristic optic nerve and visual field changes. Open-angle glaucoma is frequently called the “silent stealer of sight” because extensive optic nerve damage may occur before the patient is aware of visual field loss.

Acute Angle-Closure Glaucoma

This form of glaucoma presents with a painful red eye. The physical findings include decreased visual acuity, red eye, nonreactive pupil in middilation, markedly elevated IOP, redness, and corneal edema. Occasionally, the principal symptoms are nausea and vomiting, and, if the eye findings are overlooked, the patient may be mistaken to have abdominal or coronary disease. Patients with acute ACG require emergency treatment to lower IOP and immediate referral to an ophthalmologist. Subacute attacks of ACG may present with intermittent episodes of halos around lights or of painful blurred vision. Patients susceptible to ACG can be identified by shining a light parallel to the iris plane from the temporal side of the globe: Eyes with narrow angles will have a shadow fall on the nasal iris.

DIAGNOSIS (8)

History

A comprehensive ocular, family, and systemic history should be elicited. A history of LASIK (laser-assisted in situ keratomileusis) or photorefractive keratectomy is associated with a falsely low IOP measurement due to thinning of the cornea. The severity and outcome of glaucoma in family members, including history of visual loss from glaucoma, is of critical importance. Systemic factors, such as asthma or use of corticosteroids, may help guide treatment.

Optic Nerve Head Examination

Characteristic changes in the optic nerve and nerve fiber layer suggest early glaucomatous injury and facilitate diagnosis, as does asymptomatic elevated IOP. Cupping of the optic nerve is the pathognomonic finding of glaucoma. Changes in the contour of the optic cup in the center of the optic disk provide the first definitive evidence of glaucomatous damage. The usual cup has a round, regular contour. The cup in early glaucoma becomes notched on the superotemporal or inferotemporal rim. Later changes include an increase in the depth and width of the physiologic cup, nasal displacement of the central retinal vessels, peripapillary choroidal atrophy, and progressive pallor of the optic nerve head. Additional signs of glaucoma are asymmetric cupping and disk hemorrhages.

Assessment of disk pathology is not as straightforward as measurement of IOP. It requires greater skill, but it improves sensitivity to as much as 85%; when there is a suggestion of glaucoma, the primary physician should refer for a dilated examination of the eye to help detect early disease. Redfree illumination may aid in evaluating the retinal nerve fiber layer. Color stereophotography and computer-based image analysis of the optic nerve head and retinal nerve fiber layer are standard methods of documenting optic nerve morphology.

Measurement of Intraocular Pressure

The IOP is measured using a contact applanation method (preferably a Goldmann tonometer). It is often helpful to record diurnal IOP fluctuations, either on the same day or on different days. The presence of elevated IOP (>21 mm Hg) in the absence of cupping indicates ocular hypertension but not necessarily glaucoma. In the presence of healthy optic nerves, the degree of IOP elevation and other risk factors (age, race, family history, central corneal thickness) guide the decision to treat.

Visual Field Testing

When cupping is noted, visual field testing is indicated to check for the characteristic field deficits. Confrontation testing by the primary physician may detect large deficits, but referral for formal visual field testing is necessary for the detection of more subtle deficits. In the ophthalmologist’s office, formal testing is computerized.

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