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Glaucoma Eye Drops

IOP-lowering drops including prostaglandins, beta blockers, CAIs, and ROCK inhibitors

Glaucoma Drops: Stepwise Medication Strategy

Start with target IOP and adherence

Glaucoma pharmacotherapy works best when it is anchored to a clear target intraocular pressure (IOP) and a regimen a patient can actually follow. Most stepwise plans begin with a once-daily medication, then add a second mechanism if the patient does not reach target or if progression is suspected. As therapy escalates, technique (spacing, punctal occlusion, and bottle handling) and side-effect counseling become as important as medication selection.

Prostaglandin analogs as first-line therapy

In the absence of contraindications, prostaglandin analogs (latanoprost, bimatoprost, travoprost, and related agents) are commonly used as first-line therapy for primary open-angle glaucoma and ocular hypertension. They primarily increase uveoscleral outflow and often achieve about 25 to 30% IOP reduction with once-nightly dosing, which supports adherence compared with multi-dose regimens.

Prostaglandin-related options such as latanoprostene bunod include a nitric oxide donating component that can enhance trabecular outflow. These agents may be considered when a patient responds to a prostaglandin but has not reached target IOP on a conventional PGA alone.

Add a second mechanism when needed

If monotherapy does not achieve target IOP, additional classes are introduced stepwise. Selection should consider expected IOP effect, dosing burden, preservative exposure, and systemic contraindications.

  • Beta blockers (for example, timolol): Reduce aqueous production and can provide meaningful additional IOP lowering. Because they can be systemically absorbed, non-selective beta blockers are usually avoided in asthma, significant COPD, bradycardia, and certain cardiac conduction disorders.
  • Alpha-2 agonists (for example, brimonidine): Lower IOP by suppressing aqueous production and enhancing uveoscleral outflow. Use can be limited by allergic follicular conjunctivitis, fatigue, and dry mouth, especially with long-term use.
  • Topical carbonic anhydrase inhibitors (CAIs): Dorzolamide and brinzolamide are useful adjuncts and are often combined with other classes when additional lowering is needed, particularly when systemic CAIs are undesirable.

If two agents are needed, it is often better to add one clearly complementary mechanism and reassess rather than layering multiple drops quickly without confirming response and tolerability.

ROCK inhibitors for trabecular outflow support

Netarsudil is a rho kinase inhibitor that targets the trabecular outflow pathway by modulating the cytoskeleton within the trabecular meshwork and distal outflow system. It can be helpful when a lower target pressure is needed from a relatively low baseline, such as in normal-tension glaucoma, or as an adjunct to prostaglandin therapy. Common limiting adverse effects include conjunctival hyperemia, mild instillation discomfort, and corneal verticillata that is usually asymptomatic but should be documented and monitored.

Fixed combinations and regimen simplification

As the number of bottles increases, adherence and correct spacing of drops become harder. Fixed combinations such as timolol/dorzolamide, timolol/brimonidine, or brinzolamide/brimonidine can simplify dosing by combining two mechanisms in a single bottle. When monotherapy is insufficient, moving to an appropriate fixed combination can reduce complexity and preservative exposure compared with multiple separate bottles.

Systemic screening, technique, and follow-up

Because topical glaucoma medications can be systemically absorbed, review cardiovascular history, pulmonary disease, and current medications before prescribing agents such as beta blockers or alpha-2 agonists. Teach punctal occlusion and proper instillation technique to reduce systemic exposure and improve local efficacy. Regular follow-up remains essential to reassess target IOP, optic nerve status, and visual field stability, and to adjust therapy if progression is suspected.

Glaucoma Medications

BrandGenericDosingAmountAgesPregnancyMechanism
Alphagan P
Generic
brimonidine 0.1/0.15/0.2*%tid5/10/15mL>2 yearsBα-2 agonist↓ aqueous production↑ outflow
Azopt
Generic
brinzolamide 1%tid5/10/15mLNACcarbonic anhydrase inhibitor↓ aqueous production
Combigan
Generic
brimonidine 0.2%timolol 0.5%bid5/10/15mL>2 yearsCα-2 agonistβ blocker↓ aqueous production, ↑ outflow
Cosopt
Generic
dorzolamide 2%timolol 0.5%bid5/10mL>2 yearsCcarbonic anhydrase inhibitorβ blocker↓ aqueous production
Diamox
GenericPO
acetazolamide500mg po bid125/250mg500mg 'Sequels'>12 yearsCcarbonic anhydrase inhibitor↓ aqueous production
pilocarpine 1/2/4%qd-qid15mL>2 yearsCcholinergic agonist↑ outflow
latanoprost 0.005%qhs30 packNACprostaglandin analogue↑ outflow
Lumigan
Generic
bimatoprost 0.01/0.03*%qhs2.5/5/7.5mL>16 yearsCprostaglandin analogue↑ outflow
netarsudil 0.02%qhs2.5mLNANARho kinase inhibitor↑ outflow
netarsudil 0.02%latanoprost 0.005%qhs2.5mLNANARho kinase inhibitorprostaglandin analogue↑ outflow
brimonidine 0.2%brinzolamide 1%tid8mL>2 yearsCα-2 agonistcarbonic anhydrase inhibitor↓ aqueous production↑ outflow
Timoptic
Generic
timolol maleate 0.25/0.5%bid5/10/15mL>2 yearsCβ blocker↓ aqueous production
Travatan Z
Generic
travoprost 0.004%qhs2.5/5mL>16 yearsCprostaglandin analogue↑ outflow
Trusopt
Generic
dorzolamide 2%bid-tid5/10mL>2 yearsCcarbonic anhydrase inhibitor↓ aqueous production
latanoprostene bunod 0.024%qhs5mL>16 yearsNAprostaglandin analogue↑ outflow
Xalatan
Generic
latanoprost 0.005%qhs2.5mLNACprostaglandin analogue↑ outflow
latanoprost 0.005%(BAK free)qhs2.5mLNACprostaglandin analogue↑ outflow
Zioptan
Generic
tafluprost 0.0015%qhs30/90 packNot RecommendedCprostaglandin analogue↑ outflow

Glaucoma Medication FAQs

Why can prostaglandin analogs change eye and eyelid appearance?

Prostaglandin analogs can cause characteristic cosmetic changes over time. They may increase melanin within iris melanocytes, leading to a gradual darkening of hazel or mixed-color irides, while blue irides change less often. They can also promote eyelash growth and darken periocular skin. In some patients, long-term use is associated with a deeper upper eyelid sulcus and periorbital fat changes. These effects are usually cosmetic but can be long-lasting, so counseling is helpful, especially when only one eye is treated.

Can patients with asthma or heart disease use timolol?

Non-selective topical beta blockers such as timolol can affect heart rate and bronchial tone after systemic absorption, so they are generally avoided in asthma, significant COPD, symptomatic bradycardia, or certain conduction disorders. In selected cases, a more cardioselective option such as betaxolol may be considered with caution, but many clinicians prefer an alternative medication class. When beta blockers are used, punctal occlusion and monitoring for systemic symptoms are important.

How are medications chosen for normal-tension glaucoma (NTG)?

In normal-tension glaucoma, the goal is still to lower IOP relative to the patient's baseline while monitoring optic nerve and visual field stability. Prostaglandin analogs remain common first-line agents because of strong efficacy and once-daily dosing. Additional options include medications that can be effective at lower starting pressures, such as rho kinase inhibitors, plus selected adjuncts from other classes as needed to reach target. Some agents, including brimonidine, have been studied for possible neuroprotective effects, but clinical management still centers on IOP reduction and documented stability over time.

What is punctal occlusion and why does it matter with glaucoma drops?

Punctal occlusion is gently closing the eyelids and applying light pressure at the inner corner of the eyelids for a short period after instilling a drop. This reduces drainage through the nasolacrimal system, which can lower systemic absorption and side effects while improving local drug contact time. It is especially helpful with medications that can cause systemic effects, such as beta blockers and alpha-2 agonists.