Introduction

The goal of currently available glaucoma therapy is to preserve visual function by lowering intraocular pressure (IOP). The treatment regimen chosen should achieve this goal with the lowest risk, the fewest adverse effects, and the least disruption to the patient’s life, taking into account the cost of treatment. Although the long-term efficacy of treatment is judged by stability of the visual field, optic nerve, and other structural parameters, it is also regularly assessed by ensuring adequate IOP reduction.

The term target pressure refers to an IOP below which the clinician estimates the rate of disease progression to be sufficiently slow as to minimize the patient’s risk of experiencing further symptomatic vision loss in his or her lifetime. The value of establishing a target pressure after an initial evaluation period of a patient with glaucoma or ocular hypertension is that it encourages thoughtful appraisal of various clinical factors that influence the future risk of progression and allows for an efficient assessment of the patient’s IOP level at each subsequent visit. Even if the target pressure is achieved, the clinician must continue to evaluate the stability of structural and functional measures important in glaucoma.

Target pressure should be individualized for each eye, based on the IOP level at which damage is thought to have occurred and the severity of that damage. It can be adjusted on the basis of several factors, including the previously observed rate of progression (if known); life expectancy of the patient; and risk factors such as a history of disc hemorrhages, a thinner cornea, or a family history of severe vision loss in the setting of glaucoma (risk factors are discussed in more detail in Chapter 7 in this volume).

Evidence suggests that the severity of optic nerve injury may increase the likelihood of continued disease progression. Therefore, the more advanced the disease is on initial presentation, the lower the target pressure required to minimize the risk of further symptomatic vision loss will be. Furthermore, if severe vision loss is already present, further damage (loss of retinal ganglion cells) is likely to have a disproportionately greater impact on visual function and quality of life. Establishing a target IOP is part of the art of glaucoma management, because many different approaches can be used. Clinical trials to evaluate different approaches of determining the target pressure, or even the value of establishing a target pressure at all, are impractical to conduct; differences among groups would likely be small and would take a long period of time to detect because disease progression usually occurs slowly. In addition, simply establishing a target pressure does not guarantee it will be achieved, and it often takes a long time and many treatment adjustments to reach the target pressure.

Disease progression occurs in some patients despite reduction of IOP below the target pressure. If progression does occur at an unacceptable rate, downward revision of the target pressure may be required. Conversely, once a target pressure is established, it does not become a mandate; the risks of each sequential medical or surgical intervention thought to be required to achieve a given target pressure must be weighed against the potential benefit of further IOP reduction. Table 12-1 summarizes a general framework for estimating an appropriate target pressure; however, there is no system that would garner universal agreement.

After determining the target pressure, the clinician must decide whether to achieve this goal medically or surgically. For either approach, the anticipated benefits of any therapeutic intervention should justify the risks; regimens associated with substantial adverse effects should be reserved for patients with a high probability of progressive vision loss. In some cases, it may be necessary to accept an IOP level above the established target pressure because the adverse effects or risks of intensified therapy may be unacceptable. Both the risks and adverse events associated with specific treatment options and the risks of disease progression on the patient’s overall quality of life must be considered.

Initial treatment of ocular hypertension and most glaucomas typically involves the use of medications or laser trabeculoplasty. When starting a patient on a medication, some clinicians favor using a unilateral treatment trial in order to assess the medication’s efficacy; however, evidence suggests that this may be of limited value because of the occurrence of asymmetric IOP fluctuation between fellow eyes.

Ocular hypotensive agents are divided into several classes based on chemical structure and pharmacologic action. The classes in common clinical use include

• prostaglandin analogues, including 1 agent with a nitric oxide–donating moiety

• adrenergic drugs

  • β-adrenergic antagonists (nonselective and β1-selective)

  • adrenergic agonists (nonselective and α2-selective)

• carbonic anhydrase inhibitors (topical and systemic)

• parasympathomimetic (miotic) agents

  • direct-acting cholinergic agonists

  • indirect-acting anticholinesterase agents

• Rho kinase inhibitors

• combination medications

• hyperosmotic agents

Table 12-1 Estimating Target Pressure

Table 12-2 lists the actions and adverse effects of the various glaucoma medications. See also BCSC Section 2, Fundamentals and Principles of Ophthalmology, for additional discussion of the mechanisms of action of these medications.

• Netland PA, Tanna AP, eds. Glaucoma Medical Therapy: Principles and Management. 3rd ed. Kugler; 2020.

Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.