Chronic glaucoma

Overview

Chronic primary open-angle glaucoma (COAG) - progressive optic neuropathy from impaired aqueous outflow through the trabecular meshwork (angle remains open), causing raised IOP, optic nerve cupping, and peripheral visual field loss. Leading cause of irreversible blindness in adults >60 in the UK.

Risk Factors

Age >40

Afro-Caribbean ethnicity - earlier and more severe

Family history (first-degree relative)

Raised IOP

Thin central cornea

Normal-tension glaucoma - optic damage despite normal IOP (vascular factors)

📌

First-degree relatives of a glaucoma patient should be offered annual NHS glaucoma screening from age 40 - free of charge.

Presentation

•Characteristically asymptomatic in early/moderate stages - most detected at routine optometry

•Binocular compensation - overlapping visual fields mask unilateral peripheral defects until severe

•Peripheral visual field loss - insidious, often unnoticed until extensive

•Decreased visual acuity / central scotoma - late features only

•Increased cup:disc ratio (CDR) - >0.7 strongly suggestive; asymmetry >0.2 between eyes is significant

•Optic disc pallor - indicates nerve fibre atrophy

•Bayoneting of retinal vessels - vessels kink sharply as they dip into the deep cup

🎯

Refer to optometrist then consultant ophthalmologist if cupped optic disc or unexplained visual field defect found on examination - do not manage in primary care.

Investigations

🏆 Gold standard

•Goldmann applanation tonometry - measures IOP by force required to flatten fixed corneal area; most accurate method

•Central corneal thickness (CCT) - thin corneas cause IOP underestimation; also an independent risk factor for progression

•Automated visual field testing (perimetry) - detects peripheral defects; arcuate scotomas and nasal step defects are classic patterns

•Gonioscopy - confirms angle is open (COAG) vs closed (PACG)

•OCT of optic nerve - quantifies retinal nerve fibre layer thickness; detects structural damage before visual field loss

Management

⚠️

Treatment prevents further progression - it does NOT restore lost vision. Treat when IOP >24 mmHg with risk of visual impairment or evidence of progressive damage.

🥇 First-line

•360° selective laser trabeculoplasty (SLT) - low-energy laser improves trabecular drainage without destroying tissue; NICE NG81 recommended for IOP >24 mmHg with risk of visual impairment

•Second-line (topical drops):

•Latanoprost (prostaglandin analogue) once daily at night - increases uveoscleral outflow; side effects: increased eyelash growth, iris pigmentation, periorbital fat atrophy

•Timolol 0.5% (topical beta-blocker) twice daily - reduces aqueous production; contraindicated in asthma, COPD, significant heart block

•Dorzolamide (topical carbonic anhydrase inhibitor) - reduces aqueous production; systemic acetazolamide used in acute settings

•Brimonidine (alpha-2 agonist) - reduces aqueous production and increases uveoscleral outflow; side effects: ocular hyperaemia, fatigue

🥉 Third-line

•surgical trabeculectomy or aqueous shunt - creates new drainage channel when laser and medical therapy fail

🚨

Topical timolol eye drops can cause clinically significant systemic beta-blockade via nasolacrimal absorption - always check for asthma, COPD, or significant bradycardia before prescribing.

Complications

•Irreversible peripheral then central visual field loss - primary complication of untreated disease

•Trabeculectomy risks - hypotony, blebitis, endophthalmitis, cataract formation

•Systemic absorption of topical beta-blockers - bronchospasm or bradycardia even from eye drops