Ophthalmic Glaucoma Medications

Progressive optic nerve damage from elevated or unstable intraocular pressure is the defining risk factor in glaucoma. Medications that lower pressure slow structural loss and preserve functional vision when initiated early and titrated to a realistic target pressure. Therapy must account for diurnal fluctuation, adherence challenges, and the fact that many patients remain asymptomatic until late stages, which makes education and follow up critical to long term success.

Prostaglandin analogs such as latanoprost and bimatoprost increase uveoscleral outflow and often serve as first line therapy due to once nightly dosing and strong efficacy. Beta blockers like timolol decrease aqueous production but demand caution in asthma, COPD, bradycardia, or heart block. Alpha agonists such as brimonidine both reduce production and enhance outflow, though allergy and fatigue can limit use. Topical carbonic anhydrase inhibitors reduce production and are helpful add ons, while oral acetazolamide or methazolamide provide short term pressure control in acute spikes or when surgery is pending.

Rho kinase inhibitors like netarsudil improve trabecular outflow and lower episcleral venous pressure, offering an option when traditional classes plateau. Nitric oxide donating prostaglandin formulations further enhance outflow pathways. Fixed combinations simplify regimens, improve adherence, and reduce preservative exposure, but they limit flexibility in titrating individual components. Choose combinations when two single agents are already tolerated and dosed similarly.

Evaluate systemic history before prescribing beta blockers or oral CAIs, and monitor electrolytes and renal function if oral agents are used beyond brief courses. Prostaglandins may darken the iris and increase lash growth, effects that are cosmetic but permanent. Alpha agonists can cause follicular conjunctivitis and drowsiness, especially in children. Watch for corneal edema with CAIs in compromised endothelium and counsel all patients about transient blur or stinging after instillation.

Discuss timing (nightly versus morning), spacing multiple drops by at least five minutes, and punctal occlusion to limit systemic absorption. For patients with ocular surface disease or heavy drop burden, consider preservative free or BAK free formulations. Provide written schedules, encourage use of reminder apps or calendars, and verify the exact bottles patients are using at each visit to catch unreported substitutions or cost driven changes.

Establish an initial target pressure based on optic nerve status, visual field loss, and risk factors, then adjust as progression data accrues. Recheck IOP at different times of day to uncover peaks, repeat fields and OCT to confirm stability, and step up therapy or refer for laser or surgical options when progression occurs despite good adherence. Document medication changes, side effects, and target updates clearly so future visits can track rationale and outcomes.