The ophthalmologist should tailor ocular hypotensive therapy to the individual needs of the patient, including establishing a target IOP. Though important, IOP is only one of several factors to monitor. The effectiveness of the therapy can be determined only by careful, repeated scrutiny of the patient’s optic nerve, retinal nerve fiber layer, and visual field status (see Chapters 5 and 6).
Characteristics of the medical agents available for the treatment of glaucoma are summarized in Table 12-2. When making management decisions, ophthalmologists should consider the efficacy, adverse effect profile, and cost of the drug, as well as the likelihood of patient adherence to the drug regimen. Treatment is usually initiated with a single topical medication, unless the baseline IOP is extremely high, in which case 2 or more medications may be indicated. A discussion with the patient regarding treatment options can be beneficial for determining the optimal choice.
Prostaglandin analogues and β-blockers are reasonable choices as first-line therapy for open-angle glaucoma, as is laser trabeculoplasty in most cases. Prostaglandin analogues are the most commonly used first-line agents because of their superior efficacy, once-daily dosing, and favorable safety profile. Although the local adverse effects of β-blockers are minimal, these drugs have a greater potential for systemic adverse effects, and they lack nocturnal IOP-lowering efficacy. If prostaglandin analogues and β-blockers are contraindicated or ineffective, netarsudil (Rho kinase inhibitor), brimonidine (α2-adrenergic agonist), or a topical CAI are all reasonable options.
If 1 agent is not adequate to reduce the IOP to the desired range, the initial agent may be discontinued and another tried, or another agent can be added. Laser trabeculoplasty, if appropriate, can be considered at any point during the stepwise process of intensifying treatment, or as the initial treatment (see Chapter 13 for more information on this procedure).
For patients on a prostaglandin analogue, if a second agent is required, it is reasonable to add a β-blocker, α2-adrenergic agonist, topical CAI, or Rho kinase inhibitor. All have similar additive mean diurnal IOP-lowering efficacies, although CAIs may have better nocturnal efficacy. The decision as to which of these to select should be based on each drug’s adverse effect profile, dosing frequency, possible contraindications, and patient preference.
Again, customizing the choice of agent to the patient’s needs is helpful when selecting additional medication(s). In some circumstances, this might include parasympathomimetic agents for aphakic eyes. Clearly, when 3 or more medications are required, patient adherence to the medication regimen becomes more difficult, and the potential for local and systemic adverse effects increases. The use of fixed-combination agents can be very helpful for adherence but does not alter the adverse effect profile. Further, patients may not be able to tolerate multiple topical agents because of preservative toxicity. BAK, the agent most commonly used as a preservative, is present in most of the currently available topical ophthalmic eyedrops. If a reaction is suspected, an ocular hypotensive agent with an alternative preservative or preservative-free formulation can be used (Table 12-3).
For rehabilitation of the ocular surface, it may be beneficial to stop all topical medications—if the level of glaucomatous damage permits—and have the patient use preservative-free artificial tears frequently. During this period, the temporary use of oral CAIs may be helpful to lower IOP, if clinically warranted.
Patients sometimes fail to associate systemic adverse effects with topical drugs and, consequently, seldom volunteer symptoms. The ophthalmologist must make sure to inquire about these symptoms. In addition, communicating with the primary care physician is important not only to provide information about the potential adverse effects of glaucoma medication but also to discuss the effects that other currently prescribed medications for systemic disease might have on the glaucomatous process. Modification of oral β-blocker therapy for hypertension, for example, may affect IOP.
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.