38.4 Antiglaucoma Drugs

Glaucoma medications lower intraocular pressure (IOP) to prevent optic nerve damage and preserve vision. They do this through two main strategies: increasing the outflow of aqueous humor (the fluid inside the eye) or decreasing its production. Understanding which mechanism each drug class uses, along with its key side effects, is essential for safe administration and effective patient education.

Types and Mechanisms of Antiglaucoma Drugs

Aqueous humor is continuously produced by the ciliary body and drains out through two main pathways: the trabecular meshwork (the primary route) and the uveoscleral pathway. Every drug class below targets one or both sides of that equation.

Prostaglandin Analogs

Prostaglandin analogs (latanoprost, travoprost, bimatoprost) are typically first-line therapy for open-angle glaucoma. They work by relaxing the ciliary muscle and widening the spaces between muscle bundles, which increases uveoscleral outflow. They're dosed once daily, usually at bedtime, which helps with adherence.

Beta Blockers

Beta blockers (timolol, betaxolol, carteolol) decrease aqueous humor production by blocking beta-adrenergic receptors on the ciliary body. Timolol is nonselective (blocks both $\beta_1$ and $\beta_2$ receptors), while betaxolol is $\beta_1$-selective. That distinction matters because $\beta_2$ blockade is what causes bronchospasm, so betaxolol is the safer choice for patients with asthma or COPD.

Alpha Agonists

Alpha agonists (brimonidine, apraclonidine) have a dual mechanism: they decrease aqueous humor production by constricting ciliary body blood vessels and increase uveoscleral outflow. Brimonidine is used for long-term therapy, while apraclonidine is more commonly used short-term (e.g., to prevent IOP spikes after laser procedures).

Carbonic Anhydrase Inhibitors

These drugs inhibit the carbonic anhydrase enzyme in the ciliary body, which reduces aqueous humor production. They come in two forms:

• Topical (dorzolamide, brinzolamide): fewer systemic side effects, used as add-on therapy
• Oral (acetazolamide, methazolamide): more potent IOP reduction but significantly more systemic side effects; typically reserved for acute situations or when topical therapy isn't enough

Cholinergic Agonists (Miotics)

Cholinergic agonists (pilocarpine, carbachol) contract the ciliary muscle, which pulls open the trabecular meshwork and increases aqueous outflow through that pathway. They also constrict the pupil (miosis), which is why they're sometimes called miotics. Pilocarpine is particularly useful in acute angle-closure glaucoma because pupil constriction pulls the iris away from the drainage angle.

Rho Kinase Inhibitors

Rho kinase inhibitors (netarsudil) are a newer class. They work by relaxing cells within the trabecular meshwork itself, directly increasing outflow through that pathway. They also reduce aqueous humor production to a lesser degree. Netarsudil is typically used as adjunctive therapy.

Indications, Side Effects, and Drug Interactions

Indications

• Primary open-angle glaucoma (POAG): the most common form; most drug classes listed above are used here, with prostaglandin analogs as first-line
• Ocular hypertension: elevated IOP without optic nerve damage yet; treated to reduce the risk of progression to glaucoma
• Angle-closure glaucoma: caused by physical blockage of the drainage angle; cholinergic agonists (pilocarpine) are a key treatment because they constrict the pupil and open the angle. Carbonic anhydrase inhibitors (oral acetazolamide) are used acutely to rapidly lower IOP.

Side Effects

• Prostaglandin analogs: permanent darkening of iris color (especially in hazel/green eyes), increased eyelash growth and thickness, periorbital skin darkening, mild eye irritation. Patients should be warned about the iris color change before starting therapy.
• Beta blockers: bradycardia, hypotension, bronchospasm, fatigue, and depression. Even topical eye drops can cause systemic effects because the drug absorbs through the nasolacrimal duct into the bloodstream. Punctal occlusion after administration helps reduce this risk.
• Alpha agonists: dry mouth, fatigue, drowsiness, and ocular allergic reactions (redness, itching). Brimonidine has a relatively high rate of local allergic reactions with long-term use.
• Carbonic anhydrase inhibitors: bitter or metallic taste (topical), paresthesias/tingling in fingers and toes (oral), fatigue, and kidney stones with oral formulations. Oral forms are sulfonamide derivatives, so check for sulfa allergy.
• Cholinergic agonists: miosis causing dim vision (especially at night), brow ache, blurred near vision, and headache. Systemic cholinergic effects (bronchospasm, increased salivation) can occur but are uncommon with topical use.
• Rho kinase inhibitors: conjunctival hyperemia (eye redness) is very common, along with corneal deposits and small subconjunctival hemorrhages. These are generally mild and self-limiting.

Drug Interactions

• Beta blockers combined with calcium channel blockers (especially diltiazem, verapamil) or digoxin increase the risk of significant bradycardia and heart block. Monitor heart rate.
• Oral carbonic anhydrase inhibitors combined with thiazide or loop diuretics (furosemide) increase the risk of hypokalemia. Monitor potassium levels.
• Cholinergic agonists combined with systemic beta blockers can compound bradycardia risk.

Nursing Considerations

Monitoring and Assessment

• Measure intraocular pressure (IOP) using tonometry at baseline and at follow-up visits to evaluate whether the medication is working. The target IOP varies by patient but is generally a 20-30% reduction from baseline.
• Monitor for both local side effects (eye irritation, redness, vision changes) and systemic effects. Systemic monitoring is especially important with beta blockers (heart rate, blood pressure, respiratory status) and oral carbonic anhydrase inhibitors (electrolytes, renal function).
• Assess medication adherence at every visit. Glaucoma is often asymptomatic until significant vision loss has occurred, so patients may not feel motivated to use their drops consistently.

Collaboration and Education

• Work with ophthalmologists and optometrists to adjust therapy based on IOP response and side effect tolerability. Many patients end up on combination therapy (e.g., a prostaglandin analog plus a beta blocker).
• Reinforce that glaucoma treatment is lifelong. Stopping medication, even when IOP is well-controlled, allows pressure to rise again and damage to progress.
• Encourage regular follow-up appointments for IOP checks and optic nerve evaluation.

Patient Education

Medication Adherence and Administration

Glaucoma typically has no symptoms until vision is already lost, so patients need to understand that consistent daily use of their drops is what prevents blindness. Proper eye drop technique also matters for getting the full dose into the eye.

Steps for administering eye drops:

1. Wash hands thoroughly with soap and water.
2. Tilt the head back and gently pull the lower eyelid down to create a small pocket.
3. Hold the dropper above the eye and squeeze one drop into the pocket. Do not let the dropper tip touch the eye, eyelashes, or any surface.
4. Close the eye gently (don't squeeze it shut) and press a finger against the inner corner of the eye (punctal occlusion) for 1-2 minutes. This reduces drainage into the nasolacrimal duct and limits systemic absorption.
5. If using more than one eye drop medication, wait at least 5 minutes between drops to prevent the second drop from washing out the first.

Advise patients to report any new side effects promptly, including eye redness, irritation, vision changes (blurred vision, halos around lights), or systemic symptoms like shortness of breath or dizziness.

Lifestyle Considerations

• Stress the importance of keeping all follow-up eye appointments, even when everything feels fine.
• Recommend sunglasses with UV protection when outdoors.
• A diet rich in leafy greens (spinach, kale) and regular physical activity (like brisk walking) support overall eye health, though these do not replace medication therapy.