Glaucoma Pharmacotherapy
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Direct answer
The only variable proven to alter glaucoma outcomes is intraocular pressure, so every drug exists to lower it. In open-angle glaucoma, a prostaglandin analogue — latanoprost 0.005% once at night — is first line, being the most effective single agent with once-daily dosing. Acute angle-closure glaucoma, by contrast, an ophthalmic emergency: acetazolamide (oral or intravenous) plus topical beta-blocker and alpha-2 agonist, with pilocarpine added only once pressure has fallen, because an ischaemic sphincter will not constrict; definitive treatment is laser peripheral iridotomy. The systemic risks of eye drops — bronchospasm from timolol, apnoea from brimonidine in infants — are among the most examinable facts in ophthalmic pharmacology.
What you must remember
- Latanoprost: 0.005% once nightly; best single-agent intraocular pressure reduction; adverse effects are local — hypertrichosis of lashes, gradual iris darkening, periorbital fat atrophy; contraindicated in active uveitis and in aphakia (cystoid macular oedema).
- Timolol 0.5% twice daily: systemic absorption from the eye is enough to cause bronchospasm, bradycardia and masked hypoglycaemia — avoid in asthma, heart block, and counsel diabetics.
- Brimonidine: central alpha-2 agonist; contraindicated below two years of age because of apnoea — a classic one-liner.
- Acetazolamide: 250 mg six-hourly orally or 500 mg intravenously in the acute attack; expect paraesthesia, metabolic acidosis, hypokalaemia, urinary stones, and cross-reactivity concerns in sulphonamide allergy.
- Mannitol 20%: about 1 g/kg intravenously over 30-45 minutes if acetazolamide fails; osmotic reduction of vitreous volume in the acute attack.
- Pilocarpine timing: give 1-2% only after pressure has been lowered; constricting before that simply does not work and worsens pain.
- Never dilate a shallow anterior chamber: mydriatics precipitate angle closure — drug-induced disease by prescription.
Working through an acute angle-closure attack
A 60-year-old woman arrives with a painful, red, hazy right eye, haloes around lights, vomiting and a fixed mid-dilated pupil; intraocular pressure is 55 mmHg. The sequence defines the marks. She is made to lie supine (lens falls back slightly), given acetazolamide 500 mg intravenously, topical timolol once (checking she has no asthma), apraclonidine or brimonidine, and analgesia and antiemetics for the vomiting that otherwise defeats oral therapy. If pressure remains catastrophic at 30-60 minutes, mannitol 20% is infused. Only once pressure has meaningfully fallen — the ischaemic sphincter can finally respond — does pilocarpine 2% constrict the pupil and open the angle; giving it first is the textbook error. The fellow eye, prophylactically treated with pilocarpine and scheduled for iridotomy, shares the anatomy and will share the fate if left alone.
After the attack, the story is not over: laser peripheral iridotomy is curative for the mechanism, and the contralateral eye gets prophylactic iridotomy at the same sitting. Chronic open-angle disease then follows the opposite logic — no emergency, lifetime therapy, prostaglandin analogue at night, escalation to fixed-combination drops, and surgical options (trabeculectomy) when targets are unmet with maximal tolerated medical therapy.
Where examiners probe
The most probed idea is that eye drops are systemic drugs: an elderly asthmatic on timolol can die of bronchospasm from a drop meant for the eye, and examiners love the vignette of "wheeze after starting eye drops for glaucoma". The second trap is mechanism labelling — latanoprost increases uveoscleral outflow, timolol reduces aqueous secretion, acetazolamide reduces secretion by inhibiting carbonic anhydrase in the ciliary epithelium, and pilocarpine opens the trabecular meshwork mechanically; matching drug to mechanism is a guaranteed mark. The third is prostaglandin counselling: iris darkening is permanent and cosmetic, which matters in unilateral therapy — one brown eye and one hazel eye is a real adherence killer worth mentioning in a viva. Indian programmatic context: glaucoma screening rides on the National Programme for Control of Blindness, and generic latanoprost availability has shifted first-line practice in government hospitals away from timolol precisely because of timolol's systemic risks in the elderly.
Frequently asked questions
What is the first-line drug in open-angle glaucoma?
A prostaglandin analogue such as latanoprost 0.005% once at night — best pressure reduction, once-daily dosing, minimal systemic effects.
When is pilocarpine given in acute angle closure?
Only after intraocular pressure has been lowered medically, because the ischaemic iris sphincter cannot constrict at pressures above about 40 mmHg.
Which glaucoma drug is contraindicated in infants?
Brimonidine — it crosses to the central nervous system and causes apnoea in children below two years.
What systemic effects can timolol eye drops cause?
Bronchospasm, bradycardia, heart block and masked hypoglycaemia through systemic absorption — avoid in asthma and cardiac conduction disease.
How does acetazolamide lower intraocular pressure?
By inhibiting carbonic anhydrase in the ciliary epithelium, reducing aqueous humour production — at the cost of metabolic acidosis, paraesthesia and hypokalaemia.