INTRODUCTION — Glaucoma is most accurately defined as an optic neuropathy involving a characteristic atrophy of the optic nerve head, which may or may not be accompanied by elevated intraocular pressure (IOP). In open-angle glaucoma, optic nerve damage results in a progressive loss of retinal ganglion cell axons, which is manifested initially as visual field loss and, ultimately, irreversible blindness if left untreated . Treatment is directed at lowering IOP, regardless of baseline IOP.
This topic will focus on the treatment of primary open-angle glaucoma, where the etiology is unknown. In patients with secondary open-angle glaucoma, treatment of known causes (eg, uveitis, trauma, glucocorticoid therapy) should also be initiated in addition to lowering IOP. (See "Uveitis: Treatment" and "Major side effects of systemic glucocorticoids", section on 'Ophthalmologic effects'.)
Lowering IOP may also delay or prevent the progression to glaucoma in patients with ocular hypertension (ie, elevated IOP without optic nerve damage), which is discussed separately. (See "Open-angle glaucoma: Epidemiology, clinical presentation, and diagnosis", section on 'Management of isolated ocular hypertension'.)
Glaucoma in children, angle-closure glaucoma, and epidemiology and diagnosis of open-angle glaucoma are discussed elsewhere. (See "Overview of glaucoma in infants and children" and "Angle-closure glaucoma" and "Open-angle glaucoma: Epidemiology, clinical presentation, and diagnosis".)
GOALS OF THERAPY — The goal of therapy is to prevent further deterioration of vision from disease progression, which is accomplished by lowering the intraocular pressure (IOP). Lowering IOP has been shown to reduce the risk of progression of visual field loss and/or optic disc changes [2,3]. Lowering IOP may also delay or prevent the progression to glaucoma in patients with ocular hypertension (ie, elevated IOP without optic nerve damage), which is discussed separately. (See "Open-angle glaucoma: Epidemiology, clinical presentation, and diagnosis", section on 'Management of isolated ocular hypertension'.)
●All patients with open-angle glaucoma (as defined by the presence of optic neuropathy) should be treated with IOP-lowering therapies, regardless of their IOP at time of diagnosis. In a meta-analysis of two randomized trials of patients with open-angle glaucoma, those randomly assigned to IOP-lowering treatment were about one-third less likely to have progression of visual field and/or optic disc deterioration compared with those randomly assigned to placebo (39.2 versus 49.4 percent; hazard ratio [HR] 0.65, 95% CI 0.49-0.87) . Based on the results, seven patients with glaucoma would need to be treated to prevent one patient from progressing within five years.
●A target IOP ≥25 to 30 percent below initial IOP is a reasonable initial target that is supported by data from Early Manifest Glaucoma Trial (EMGT) and the Collaborative Initial Glaucoma Treatment Study (CIGTS) [4-6]. The EMGT study found a graded effect of IOP lowering and risk of visual field loss .
Therapy must be individualized, taking into account the patient's disease state, target pressure, and medical comorbidities. There are no standard guidelines for the optimal target IOP. The treating clinician typically defines a target pressure at which no further damage is likely to occur for that eye. As open-angle glaucoma can be asymmetric or even monocular, ophthalmologists must determine appropriate target pressures for individual patients and individual eyes, with adjustments based on close follow-up of visual fields and evaluation for cup progression. The target pressure must be lowered if nerve damage occurs despite achieving the target. Typically, patients with more advanced disc damage and field loss need lower target pressures.
●Treatment strategies for patients with normal-pressure glaucoma are generally the same as for patients with high-pressure glaucoma [4,7]. A target IOP ≥25 to 30 percent below the initial IOP is reasonable in this setting as well.
●Patient education, informed participation in decision-making, and emphasis on adherence are particularly important, since open-angle glaucoma is largely asymptomatic. (See 'Medication adherence and compliance' below.)
Other factors such as blood supply, nerve metabolism, and extracellular matrix likely play a role in the progressive optic neuropathy of glaucoma . However, treatment targeting these other factors in patients with open-angle glaucoma has not been well studied .
CHOOSING THERAPY — All patients with glaucoma should receive treatment upon diagnosis. Pharmacologic therapy, laser therapy (trabeculoplasty), and/or surgery (trabeculectomy) have been shown to lower intraocular pressure (IOP) in randomized trials (discussed below) [10-14]. However, there are little data on their efficacy in preventing deterioration of visual acuity. A limitation of available evidence is the dual challenge of accounting for ongoing advances in all three therapeutic strategies and assessing a key outcome, visual deterioration, that may take many years to develop. (See 'Types of therapy' below.)
●For most patients, we use pharmacologic or laser therapy as first-line treatment of open-angle glaucoma, especially in view of increased risk of complications associated with surgical therapy (scarring, cataract formation, and other potentially vision-threatening complications) [11,14,15]. (See 'Surgery' below.)
The choice for initial laser versus pharmacologic therapy is best made through collaborative decision-making between patient and doctor. Outcomes are equivalent . Patients who have difficulty with adherence to eyedrop therapy due to expense or intolerance, or who simply desire to avoid daily medication use, may choose to have laser therapy. Patients who wish to avoid a procedure may choose pharmacologic therapy.
Close follow-up of IOP is required regardless of which treatment is chosen. Even with laser treatment, the desired reduction in IOP may not be achieved and, if achieved, the reduction typically lasts for only one to five years .
●We consider surgical therapy a first-line approach only for patients with severe visual field loss at baseline, and a second-line approach for patients with advanced open-angle glaucoma who do not respond to medications or laser therapy .
TYPES OF THERAPY — The majority of data regarding the efficacy of treatment are presented in terms of the absolute lowering of intraocular pressure (IOP), a surrogate marker for prevention of glaucoma progression and vision loss. Results are rarely presented as the percentage of patients who meet their individual IOP reduction goals, or who have reduced deterioration of vision, the latter being a long-term outcome difficult to assess in most trials.
●Mechanism of action – Topical medications work either by increasing aqueous outflow (prostaglandins, alpha adrenergic agonists, cholinergic agonists, rho kinase inhibitor) or by decreasing aqueous production (alpha adrenergic agonists, beta blockers, carbonic anhydrase inhibitors) (table 1). Systemic carbonic anhydrase inhibitors also decrease aqueous production.
●Dosing and administration – Pharmacologic therapy often requires administration of multiple medications multiple times per day. Many older drugs require dosing three or four times a day. Newer drugs can be administered once or twice daily, but these drugs can be expensive.
Combining drops from different classes (ie, beta blocker plus prostaglandin, or beta blocker plus carbonic anhydrase inhibitor) can cause a greater reduction in the IOP than monotherapy [19-22], and several drugs are available as fixed combination products. Adding a second medication is reasonable if initial monotherapy is not effective. In one trial comparing the fixed combination of latanoprost and timolol with each agent as monotherapy, 74 percent of those using the combination therapy had a diurnal IOP reduction of 30 percent or more at 12 weeks, compared with 58 and 33 percent of those treated with latanoprost and timolol alone, respectively .
Bottles containing ophthalmic drops generally have different color caps depending on the pharmacologic class. These colors differ substantially between countries. Clinicians should check bottles to ensure proper administration when patients are prescribed more than one topical ophthalmic medication.
●Side effects – Glaucoma medications have potential side effects and may be particularly inconvenient to use for some older adult or incapacitated patients. Side effects of specific medications are reviewed below.
Prostaglandins (preferred therapy) — The topical prostaglandins are increasingly chosen as initial monotherapy in open-angle glaucoma and have been consistently shown to be effective at lowering IOP and well tolerated [18,21,23-26]. Prostaglandins have the advantage of once-daily dosing and do not have the risk of systemic side effects seen with topical beta blockers.
Ocular side effects of prostaglandins include hyperemia, eye irritation, orbital fat atrophy, increase in the number and length of eyelashes, and changes in iris and lash pigmentation; the latter two are more easily noticed if only one eye is treated. Different prostaglandins may differ in side effects. In one network meta-analysis of randomized trials, latanoprost had the lowest mean proportion of patients with hyperemia (24 percent) while bimatoprost had the highest (59 percent) .
Local irritation (itching and dryness) may be due to corneal irritation from benzalkonium chloride, used as a preservative in several preparations. Tafluprost contains no preservative; however, refrigeration and care in handling the single-use packets is needed to minimize risk of infection, with immediate discard of any unused solution .
Proprietary prostaglandins are expensive, which may impact drug adherence, but generics are available.
Most meta-analyses have found prostaglandins to be more effective at lowering IOP than beta blockers, carbonic anhydrase inhibitors, and alpha adrenergic agonists for the treatment of open-angle glaucoma [13,21,23,28].
As an example, in a 2016 network meta-analysis of randomized trials evaluating medical treatments for over 20,000 patients with primary open-angle glaucoma, bimatoprost (a prostaglandin) was the most effective at lowering the mean IOP at three months (5.61 mmHg, 95% CI 4.94-6.29) compared with levobunolol, the best performing beta blocker (4.51 mmHg, 95% CI 3.85-5.24) . The most effective alpha adrenergic agonists and carbonic anhydrase inhibitors produced lower mean IOP decreases (3.59 and 2.49 mmHg respectively).
Beta blockers — Beta blockers may be appropriate as initial therapy for those patients who cannot afford a topical prostaglandin. Like prostaglandins, topical beta blockers (eg, timolol, betaxolol) have a long duration of action which allows for once- or twice-daily dosing. They are associated with few ocular side effects, although some patients have hyperemia or a burning sensation in the eyes [29-31].
In the network meta-analysis discussed above , the mean reductions in IOP at three months for beta blockers ranged from 4.51 mmHg (95% CI 3.85-5.24) for levobunolol to 2.24 mmHg (95% CI 1.59-2.88) for betaxolol, which is slightly less than the reduction (5.61 mmHg) observed with the most effective prostaglandin.
In contrast to prostaglandins, which have an excellent profile as far as lack of systemic side effects or contraindications, topical beta blockers are contraindicated in some patients with pulmonary or cardiac disease. In these patients, side effects are similar to those associated with systemic beta-blocker therapy including worsening of heart failure, bradycardia, heart block, and increased airway resistance. Airway obstruction has been reported with topical beta-blocker therapy even in patients who do not have a history of airway disease [32,33]. Other potential side effects of topical beta-blocker therapy include exercise intolerance, depression, and sexual dysfunction. (See "Major side effects of beta blockers".)
●Alpha adrenergic agonists (eg, brimonidine) appear to be similarly effective to beta blockers in lowering IOP in open-angle glaucoma, but they are associated with a number of ocular side effects including allergic conjunctivitis, hyperemia, and ocular pruritus . The nonselective agents (epinephrine) also may be associated with arrhythmia, hypertension, and tachycardia. These agents might be considered when there is intolerance or formulary or cost issues, or in combination with the preferred agents if adequate control is not achieved.
●Topical carbonic anhydrase inhibitors do not appear to be as effective in treating open-angle glaucoma compared with other pharmacologic therapy . In the meta-analysis described above , the most effective carbonic anhydrase inhibitor (dorzolamide) produced a mean IOP decrease at three months of 2.49 mmHg (95% CI 1.85-3.13). These agents might be considered when there is intolerance or formulary or cost issues with the preferred agents, or in combination if adequate control is not achieved.
●Cholinergic agonists have fewer systemic adverse effects than beta blockers, but ocular side effects such as fixed, small pupils, myopia, and increased subjective visual disturbance related to coexistent cataract have decreased the utilization of these drugs, especially over the last three decades as prostaglandins, alpha adrenergic agonists, and topical carbonic anhydrase inhibitors became available. These agents are now rarely used except in low-resource settings where newer drugs may be too expensive or unavailable.
●Combination products are available for several classes of drugs, in various combinations (eg, latanoprost-timolol, travoprost-timolol, dorzolamide-timolol, brimonidine-timolol, brinzolamide-timolol, brinzolamide-brimonidine, netarsudil-latanoprost). Such combinations should not be used as initial treatment, but for patients requiring treatment with two of these drug classes they offer convenience and cost advantages. Which combinations are available where depends on national differences in drug approval and regulation.
●Netarsudil was approved in 2017 by the US Food and Drug Administration (FDA) for topical use for open-angle glaucoma or ocular hypertension . Netarsudil is a rho kinase inhibitor; it is believed to reduce IOP by increasing the outflow of aqueous humor through the trabecular meshwork. Licensing studies suggested that netarsudil is noninferior to timolol. A 2022 systematic review of 17 trials concluded that the ocular hypotensive effect of netarsudil may be inferior to latanoprost and slightly inferior to timolol in patients diagnosed with ocular hypertension or open-angle glaucoma .
Laser therapy — Laser therapy (trabeculoplasty) increases aqueous outflow by improving drainage of aqueous humor through the trabecular meshwork. The procedure is performed as an outpatient in the ophthalmologist’s office or at a surgicenter or hospital outpatient clinic.
Options include argon laser trabeculoplasty or selective trabeculoplasty, which uses a low-level laser that only affects selected pigmented tissue in the eye. There is a trend toward preference for selective laser trabeculoplasty (SLT) over argon laser trabeculoplasty due to fewer adverse events such as pressure rise attributed to scarring, ease of use, and the fact that the procedure can be repeated .
Efficacy compared with pharmacologic therapy — In a 2011 review of the literature prepared for the American Academy of Ophthalmology, the long-term efficacy of initial argon laser trabeculoplasty was found to be comparable with initial medical therapy (eye drops) for open-angle glaucoma .
Subsequent trials have confirmed the efficacy and cost-effectiveness of SLT compared with medical therapy. As an example, in a trial in the United Kingdom (LiGHT) including 718 patients with treatment-naïve open-angle glaucoma who were randomized to SLT (followed by eye drops if needed) or eyedrop treatment alone, both groups had similar health-related quality of life after three years . In secondary outcomes, the laser group had better IOP stability and required fewer surgeries to lower IOP (0 versus 11) compared with the eyedrop group. Of the patients treated with laser therapy, 74 percent required no eye drops at three years. Laser therapy was more cost-effective than eye drops as an initial treatment.
In a 2020 meta-analysis of eight trials (including the LIGHT trial) comparing SLT with medication-only therapy for open-angle glaucoma among 1229 patients, no significant differences were found between the treatments as far as reduction or control of IOP, and the SLT group required fewer medications . A subsequent 2022 meta-analysis found moderate evidence of a small benefit from laser therapy in slowing visual field loss compared with medication .
The potential cost-saving of laser treatment is related to the cost of the procedure and of medication . A United States modelling study found that initial laser therapy might be slightly more cost-effective than medical therapy if, as expected, medical adherence in community settings is lower than reported in clinical trials, but that medication provides somewhat greater value assuming optimal adherence .
Surgery — We use surgical therapy as a first-line approach only for patients with severe visual field loss at baseline, and as a second-line approach for those patients with advanced open-angle glaucoma who have not responded to medications or laser therapy.
Surgical therapy is associated with a number of attendant risks including cataract formation, scarring, and potentially vision-threatening complications such as over-filtration, hypotony, and infection . In a trial of patients randomized to receive medical or surgical treatment for glaucoma, the five-year cumulative probability of cataract extraction was greater in those treated with surgery (19.0 percent) than medication (6.5 percent) .
Surgical therapy (trabeculectomy) involves the creation of a filtration bleb to allow egress of aqueous humor from the eye. This is an alternative route to the normal pathway via the trabecular meshwork and the canal of Schlemm (figure 1). Trabeculectomy may fail because of excessive scar tissue formation. There are reports of the use of anti-scarring adjuncts before, during, or after surgery, such as beta irradiation and antimetabolites (5-fluorouracil and mitomycin), to increase the rate of surgical success [42,43]. There is great variation in use and choice of adjuncts worldwide, and adjuncts can be associated with a higher complication rate. For example, beta irradiation at the time of trabeculectomy can minimize scar tissue formation and increase the likelihood that surgery will effectively lower the IOP, but it increases the risk of cataract formation . Successful repeat trabeculectomy using topical mitomycin adjunctively has been reported in patients who do not achieve or sustain normal IOP readings with their initial surgery .
Glaucoma surgery sometimes involves the placement of mechanical shunts (also called "valves"). Shunts are typically only placed in patients with advanced disease in whom medical and laser therapies are inadequate and who have an underlying diagnosis that increases the risk of failure of conventional surgery (eg, neovascular glaucoma, cornea transplant, iridocorneal endothelial [ICE] syndrome). An expanding role for shunts may be emerging, including use in eyes that have had previous conjunctival incisions (cataract extraction, retinal surgery, or prior failed trabeculectomy). A 2017 meta-analysis that included three randomized trials (380 patients; very low-quality evidence) found that the IOP was not different in patients who underwent aqueous shunt compared with trabeculectomy (mean difference 2.55 mmHg, 95% CI -0.78 to 5.87) . Visual acuity and number of antiglaucoma medications needed were also not different between the groups. The largest trial reporting outcomes at five years found that, while the IOP and visual acuity were similar in both groups, fewer patients receiving a shunt required reoperation compared with those who underwent trabeculectomy (9 versus 29 percent, respectively) .
There is a group of interventions emerging called “minimally invasive glaucoma surgery” (MIGS), which offers promise as a less risky approach to surgical control of glaucoma progression . Based on data from Cochrane reviews, some MIGS may afford patients with glaucoma greater medication-free disease control than cataract surgery alone .
Frequency and duration — Patients with open-angle glaucoma, regardless of whether they are treated with medications, laser, or surgical treatment, require lifetime therapy and monitoring of intraocular pressure (IOP), the optic disc, and visual fields. Some ophthalmologists also use optical coherence tomography, which may be more sensitive than visual field testing in identifying progression in early glaucoma . Patients who undergo glaucoma surgery also require regular monitoring for failure of the filtration bleb and the development of cataracts. (See 'Surgery' above.)
The appropriate interval for follow-up varies based upon the extent of damage, whether or not there is recent disease progression, the stability of IOP control, and the level of adherence with medical therapy and follow-up care. Most patients with open-angle glaucoma are seen by the ophthalmologist at least twice yearly, as long as they are stable. (See 'Progression during monitoring' below.)
Progression during monitoring — Patients with progressive disease require closer assessment by the ophthalmologist, as often as every one to three months. When there is evidence of progression, the next step is to reduce the IOP further by adding or changing pharmacologic agents or by performing laser therapy or surgery. Clinical decision-making in the management of progressive disease is beyond the scope of this topic.
Medication adherence and compliance — The therapy of open-angle glaucoma is often characterized by poor adherence to prescribed therapies because the disease is asymptomatic for many years and eyedrops can be difficult to use. In a cross-sectional observational study of over 1000 patients on a variety of topical and oral therapies, 24.7 percent were nonadherent, with nonadherence associated with male sex and increased dosing frequency of the prescribed medications .
If primary care providers become aware that a patient has not been adherent to their topical regimen for glaucoma, it is best to engage the patient in a discussion of why this is the case, and to refer them to an ophthalmologist for reevaluation and discussion of treatment options.
As discussed above, bottles containing ophthalmic drops generally have different color caps depending on the pharmacologic class. These colors differ substantially between countries. Clinicians should check bottles to ensure proper administration when patients are prescribed more than one topical ophthalmic medication.
USE OF MEDICATIONS WITH GLAUCOMA WARNINGS — There are many medications that carry warnings or contraindications regarding use in patients with glaucoma. These warnings and contraindications are relevant regardless of whether or not the patient is taking glaucoma medications; they are not drug-drug interactions.
These warnings can pose difficulties for clinicians, as potential adverse outcomes vary according to the type of glaucoma (open- versus narrow-angle) and the type of laser treatment (iridotomy versus trabeculoplasty). Iridotomy may protect against certain medication effects, but its protective effect varies among patients, as well as over time, and requires ophthalmological confirmation.
The most clinically relevant specific glaucoma interactions are discussed below by drug type. Ophthalmologic consultation is suggested when prescription of these agents is being considered in patients with glaucoma.
Glucocorticoids — Glucocorticoid preparations (ie, ocular, oral, inhaled, and periocular dermatologic preparations) can raise intraocular pressure (IOP) in open-angle glaucoma patients. For example, 90 percent of primary open-angle glaucoma patients have been reported to develop an elevation in pressure after one month of topical ocular use . Intranasal steroids (despite carrying a warning about use in glaucoma) typically do not cause an increase in IOP .
In general, a two-week (or longer) course of glucocorticoids is required before an increase in IOP is seen. The mechanism is not well established but is thought to be related to reduced outflow at the trabecular meshwork. A glucocorticoid-induced increase in IOP is sometimes referred to as a “steroid response.”
Typically, the pressure goes up when a threshold of dose and duration is reached, although this threshold varies from patient to patient. Additionally, for an individual patient, the threshold tends to get lower with additional courses of glucocorticoid treatment. Therefore, once a steroid response is triggered, providers must be vigilant against further steroid responses at even lower doses or duration of therapy. Patients known to have an increase in IOP with topical ocular glucocorticoids are at increased risk of pressure rise with other preparations.
Dermatologic preparations can raise IOP if they are used on the lids, particularly with chronic use such as in atopic dermatitis. These patients require close monitoring by an ophthalmologist, and use of alternative calcineurin inhibitors should be considered. (See "Treatment of atopic dermatitis (eczema)", section on 'Topical calcineurin inhibitors'.)
Elevation in IOP has also been reported with application of glucocorticoids on skin that was not periocular, either from ocular contamination or systemic absorption, although this is rare . Glaucoma patients should be advised to wash their hands after applying dermatologic steroids or to use gloves.
Guidance — Guidance for consideration of ophthalmologic evaluation during glucocorticoid treatment in patients with open-angle glaucoma is as follows:
●All patients with primary open-angle glaucoma can be safely treated with a short course (less than two-weeks’ duration) of any glucocorticoid preparation without ophthalmologic evaluation.
●Patients prescribed a course of oral, inhaled, ocular, or topical periocular glucocorticoids of longer than two weeks should be seen by their treating eye doctors within three to four weeks of initiating such treatment. The same applies to any increase in glucocorticoid therapy for patients being treated or monitored for glaucoma.
●It is not sufficient to have “a pressure check” by someone not familiar with the extent of glaucoma, as the target pressure for that particular patient may be lower than what is the high end of the normal range for IOP in patients with normal optic nerves and fields.
In addition, patients without a history of glaucoma but who are at increased risk because of treatment with chronic oral glucocorticoids at any dose, pulmonary inhaler, or potent topical glucocorticoid to the face (especially the eyelids) should have comprehensive eye evaluations to detect steroid response at least annually.
Systemic sympathomimetics — Systemic sympathomimetics include ephedrine and pseudoephedrine-containing drugs sold over the counter for upper respiratory tract congestion, tricyclic antidepressants, antipsychotics, and, to a lesser degree, selective serotonin uptake inhibitors.
Patients with narrow angles or those who have had laser iridotomy as prophylaxis against angle closure may experience angle-closure glaucoma with these medications . The mechanism is pupillary block related to dilation of the pupil. These medications should not be prescribed to such patients unless approved by their ophthalmologist.
In other patients, including those with primary open-angle glaucoma, these agents can cause temporary mydriasis (pupillary dilation) with no major consequences.
Systemic anticholinergics — Systemic anticholinergic drugs have a potential adverse effect on patients with narrow angles but no effect on patients with primary open-angle glaucoma. Systemic anticholinergics include anticholinergic inhalers, overactive bladder medications, antihistamines, and some drugs used for muscle spasms.
Eyedrops for allergic conjunctivitis — Sympathomimetic or anticholinergic eye drops available over the counter or by prescription for allergic conjunctivitis have a potential adverse effect on patients with narrow angles but no effect on patients with primary open-angle glaucoma.
PREVENTION — Glaucoma is a leading cause of blindness worldwide. Although the disease cannot be prevented, early diagnosis and initiation of treatment can prevent or delay visual loss. Screening for glaucoma is discussed in detail elsewhere. (See "Open-angle glaucoma: Epidemiology, clinical presentation, and diagnosis", section on 'Screening'.)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
SUMMARY AND RECOMMENDATIONS
●Goals of therapy – The goal of therapy is to prevent further deterioration of vision from disease progression, which is accomplished by lowering the intraocular pressure (IOP). IOP can be lowered by pharmacologic therapy, laser therapy, and/or surgery. (See 'Goals of therapy' above.)
•For patients with open-angle glaucoma, we recommend treatment to lower IOP (Grade 1B). Lowering IOP has been shown to reduce progression of visual field loss and/or disc deterioration in patients with and without increased IOP. (See 'Goals of therapy' above.)
●Choosing initial therapy – For most patients, pharmacologic or laser therapy is the first-line treatment. However, if there is already significant visual loss at the time of presentation, surgery is reasonable as a first-line treatment. (See 'Choosing therapy' above.)
•Laser versus pharmacologic therapy – The choice for initial laser versus pharmacologic therapy is best made through collaborative decision-making between patient and doctor. Initial laser treatment may be best in patients who have difficulty with adherence to eyedrop therapy due to expense, desire to avoid daily medication use, or other reasons. For patients who wish to avoid procedures, pharmacologic therapy is an effective alternative. Close follow-up is required regardless of which treatment is chosen, as the effect of laser treatment is not permanent. (See 'Choosing therapy' above.)
•Prostaglandins as first-line therapy – If pharmacologic therapy is chosen, we suggest topical prostaglandins as first-line pharmacologic therapy rather than other topical medications (Grade 2C). Prostaglandins have lower rates of systemic side effects and may have somewhat better efficacy than beta blockers. (See 'Prostaglandins (preferred therapy)' above.)
•Combination therapy if needed – Combining drops from different classes (ie, beta blocker plus prostaglandin or beta blocker plus carbonic anhydrase inhibitor) can cause a greater reduction in the IOP than monotherapy. Adding a second medication is reasonable if initial monotherapy is not effective. (See 'General principles' above.)
●Monitoring – The target IOP and subsequent monitoring intervals depends on several factors, including the extent of optic nerve damage, whether or not there is recent progression of damage, the stability of IOP, and the level of patient adherence. A target IOP ≥25 to 30 percent below initial IOP is a reasonable initial target. (See 'Monitoring' above and 'Goals of therapy' above.)
●Medications with glaucoma warnings – Certain medications with glaucoma warnings require ophthalmologic evaluation prior to or during use. (See 'Use of medications with glaucoma warnings' above.)
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