Glaucoma Drugs

Glaucoma drugs lower intraocular pressure, the only modifiable risk factor for optic nerve damage. They act by reducing aqueous humour production or increasing its outflow. Treatment starts with a single agent, adding or switching depending on target pressure, and is lifelong in open-angle disease. Adherence is the main limit to success.

Mechanism. Prostaglandin analogues increase uveoscleral outflow; beta blockers, carbonic anhydrase inhibitors and alpha 2 agonists reduce aqueous production (alpha 2 agonists also increase uveoscleral outflow); miotics increase trabecular outflow; rho kinase inhibitors increase trabecular outflow; osmotic agents draw water out of the vitreous for emergency use.

Pharmacokinetics. Topical drops reach the aqueous humour after corneal penetration and also drain through the nasolacrimal duct to the nose, where they are absorbed systemically without first-pass metabolism. Nasolacrimal occlusion or eyelid closure for 2 to 3 minutes after instillation reduces systemic absorption.

Fixed combinations (timolol with dorzolamide, brimonidine, latanoprost or travoprost; brimonidine with brinzolamide) simplify regimens and halve the preservative load.

Open-angle glaucoma. Set a target pressure (often a 30 to 40 percent reduction from baseline in moderate disease, lower in advanced disease). First choice is a prostaglandin analogue once daily; add a beta blocker if the target is not reached, then a carbonic anhydrase inhibitor or alpha 2 agonist. Use a fixed combination when two drugs are needed. Move to laser trabeculoplasty or surgery if disease progresses on maximum tolerated therapy.

Instillation technique. Use one drop at each instillation, wait 5 minutes between different drops, close the eyes and press the inner corner for 2 to 3 minutes, and apply ointments last. Bottles last about 4 weeks after opening.

Acute angle closure. Emergency treatment lowers pressure while preparing for laser peripheral iridotomy: acetazolamide 500 mg orally or by intravenous injection, a topical beta blocker, a topical alpha 2 agonist and topical steroid; give pilocarpine only once pressure has begun to fall; add mannitol by intravenous infusion if pressure remains very high. Give analgesia and an antiemetic.

Other uses. Ocular hypertension without damage, after laser or surgery for pressure spikes, neovascular glaucoma (with treatment of the cause), and normal-tension glaucoma (pressure lowering of about 30 percent).

Selection. Choose by systemic disease (avoid beta blockers in asthma, heart block; avoid alpha 2 agonists in young children), pregnancy plans, adherence, cost and local availability.

Class effects. Ocular surface disease from preservatives (benzalkonium chloride) causes stinging, dry eye and poor adherence; use preservative-free preparations in severe cases. Systemic absorption causes cardiopulmonary effects with beta blockers and central nervous system effects with alpha 2 agonists.

Monitoring. Pressure checks every 3 to 6 months once stable, visual field testing and optic nerve assessment at least yearly, and review of adherence and drop technique at every visit. Add a drug and assess response after 4 to 6 weeks; stop a drug that gives less than a 15 percent pressure fall.

Special groups. Pregnancy: timolol and brimonidine are used with care; prostaglandin analogues are used when benefit outweighs risk; laser is preferred. Children: specialist care, usually surgical. Older adults: simplified once-daily regimens.

Region: primary open-angle glaucoma is common and often severe and late at presentation in East Africa, so early laser trabeculoplasty or surgery is often better than lifelong drops where adherence, distance from services and cost are barriers; generic latanoprost and timolol are the usual first choices; traditional eye remedies can cause harm and delay care.