Glaucoma — Symptoms, Causes & Treatment | MyMedicPlus

Glaucoma is a group of progressive optic neuropathies characterised by structural damage to the optic nerve head and retinal nerve fibre layer (RNFL), with corresponding visual field loss, most commonly associated with elevated intraocular pressure (IOP). It is the leading cause of irreversible blindness worldwide, affecting approximately 80 million people, with 8 million bilaterally blind — and prevalence is projected to reach 111 million by 2040 as populations age. Primary open-angle glaucoma (POAG), the most common form (approximately 70% of cases), progresses insidiously without pain or symptoms until advanced visual field loss has occurred — patients may lose 40% or more of retinal ganglion cells before noticing any change in vision. Acute angle-closure glaucoma, by contrast, presents dramatically with sudden severe eye pain, headache, and rapidly failing vision. Normal-tension glaucoma (NTG — IOP within the statistical normal range of 10–21 mmHg despite progressive optic nerve damage) accounts for 30–40% of POAG in Western populations and up to 90% in Japanese populations. Elevated IOP above 21 mmHg is the principal modifiable risk factor, and IOP reduction by any mechanism — drops, laser, or surgery — is the only proven strategy to slow or halt glaucomatous progression. Glaucoma is largely asymptomatic until irreversible damage is advanced, making routine screening critical for at-risk populations.

In primary open-angle glaucoma (POAG — the most common form, accounting for 60–70% of all glaucoma in Western countries), aqueous humour outflow resistance is increased at the level of the trabecular meshwork and Schlemm's canal, leading to raised IOP. The mechanisms are incompletely understood but involve accumulation of extracellular matrix material, loss of trabecular endothelial cells, and reduced phagocytic activity within the meshwork. Normal-tension glaucoma (NTG) — a subset of POAG where optic nerve damage occurs despite IOP consistently within the statistically normal range (10–21 mmHg) — accounts for 30–40% of all POAG and up to 90% of glaucoma cases in East Asian populations (Japan, Korea); vascular dysregulation (particularly nocturnal hypotension impairing optic nerve blood flow), CSF pressure abnormalities, and direct neuro-toxic mechanisms are implicated. Primary angle-closure glaucoma (PACG): occurs when the peripheral iris physically apposes or adheres to the trabecular meshwork, blocking aqueous outflow — hyperopic eyes (short axial length), shallow anterior chamber, and thick iris are anatomical risk factors; PACG is more common in East Asian, Inuit, and South Asian populations and causes more blindness globally than POAG despite lower prevalence, due to more severe and acute presentations. Secondary glaucomas: pseudoexfoliation glaucoma (fibrillar material deposition on the lens and trabecular meshwork — the most common secondary glaucoma worldwide; 6-fold elevated IOP and high risk of optic nerve damage); pigment dispersion syndrome (melanin granules from iris posterior surface deposited in the trabecular meshwork); neovascular glaucoma (secondary to proliferative diabetic retinopathy or central retinal vein occlusion — new vessels in the angle cause fibrovascular membrane blocking outflow); steroid-induced glaucoma (any route: topical, inhaled, systemic — IOP elevation in 6% of the population with high-dose topical steroids; 'steroid responders'). Elevated IOP is the primary modifiable risk factor — each 1 mmHg reduction in IOP reduces glaucoma progression risk by approximately 10–13% (Collaborative Normal-Tension Glaucoma Study, European Glaucoma Prevention Study).

Primary open-angle glaucoma (POAG) is characteristically asymptomatic — it is a 'silent thief of sight' — progressing unnoticed until central vision is threatened. The disease begins with peripheral (arcuate) visual field loss that the patient cannot detect because binocular peripheral vision is preserved by the fellow eye filling in the scotoma, and because by the time visual field defects are detectable by standard automated perimetry (SAP/Humphrey visual field), approximately 25–35% of retinal ganglion cells have already been irreversibly lost. Central visual acuity is preserved until very advanced disease, making self-detection virtually impossible without regular eye examination. Subtle early symptoms occasionally reported: slight blurring around lights (halos) in those with concurrent lens changes; mild monocular visual disturbances. Acute angle-closure glaucoma (AACG) — the dramatic exception: presents with severe, throbbing ocular pain (one of the most painful ophthalmological conditions); profound visual disturbance and blurring; halos around lights from corneal oedema; headache (often severe, frontal or periorbital — misdiagnosed as migraine or cluster headache); nausea and vomiting (vagal response to severe pain — misdiagnosed as gastroenteritis). On examination: conjunctival injection (red eye — ciliary flush — circumcorneal injection), cloudy cornea (microcystic oedema from acutely elevated IOP), fixed mid-dilated pupil (sphincter ischaemia from high IOP preventing miosis), shallow anterior chamber, and markedly elevated IOP (50–80 mmHg — normal 10–21 mmHg). AACG is an ophthalmological emergency — sustained IOP above 50 mmHg causes irreversible optic nerve damage within hours and permanent vision loss within 24–48 hours without treatment.

Comprehensive glaucoma evaluation integrates multiple investigations as no single test is sufficient to diagnose or stage the disease. Intraocular pressure (IOP) measurement: Goldmann applanation tonometry (GAT) — the gold standard measurement technique, performed at the slit lamp — measures the force required to applanate a 3.06 mm diameter disc of cornea; normal range 10–21 mmHg; single IOP measurement is unreliable (diurnal IOP variation of up to 6 mmHg in glaucoma patients — typically highest on waking); pachymetry (central corneal thickness — CCT) is required to interpret GAT readings (thin corneas give falsely low readings; thick corneas give falsely high readings — correction formulae apply). Optic disc examination (slit lamp biomicroscopy with 78D or 90D lens): cup-to-disc ratio (CDR) — the ratio of the excavated cup to the total disc diameter; normal CDR is 0.3 in most individuals; CDR above 0.7 or asymmetric CDR (above 0.2 asymmetry between eyes) warrants full glaucoma investigation; focal neuroretinal rim (NRR) thinning (particularly inferior and superior poles following the ISNT rule — Inferior, Superior, Nasal, Temporal — in decreasing order of normal NRR thickness); disc haemorrhages (small splinter haemorrhages at the disc margin — highly specific for glaucomatous progression). Optical coherence tomography (OCT): the cornerstone of modern glaucoma monitoring — measures retinal nerve fibre layer (RNFL) thickness around the optic disc in microns (normal average 100 μm; glaucomatous loss causes thinning below 80 μm; temporal quadrant thinning below 60 μm indicates advanced disease); ganglion cell complex (GCC) analysis provides additional detection sensitivity; OCT detects structural damage 5–10 years before visual field defects are detectable by perimetry ('pre-perimetric glaucoma'). Standard automated perimetry (SAP — Humphrey Visual Field analyser, 24-2 threshold): maps the visual field; SITA Standard or SITA-SWAP algorithms; glaucoma produces characteristic arcuate defects (superior and inferior Bjerrum scotomas), nasal steps, and temporal wedge defects corresponding to areas of RNFL loss. Gonioscopy (examination of the anterior chamber angle using a mirrored contact lens): mandatory in all glaucoma suspects — distinguishes open angle from narrow/closed angle, assesses angle anatomy and pigmentation, and detects secondary causes (neovascularisation, pseudoexfoliation, pigment dispersion). Central corneal thickness measurement.

All glaucoma treatments aim to lower IOP to prevent or slow progressive optic nerve damage and visual field loss. Treatment targets are individualised — a 'target IOP' is calculated based on baseline IOP, stage of glaucoma (disc and field damage), age, life expectancy, and rate of progression; the Advanced Glaucoma Intervention Study showed that reducing mean IOP below 18 mmHg in early to moderate glaucoma halted progression in 90% of patients. Topical IOP-lowering medications — first-line treatment: Prostaglandin analogues (PGAs — latanoprost 0.005% once nightly; bimatoprost 0.03% once nightly; travoprost 0.004% once nightly; tafluprost; latanoprostene bunod — Vyzulta): the most effective IOP-lowering agents, reducing IOP by 25–35% from baseline by enhancing uveoscleral outflow; well-tolerated; side effects include conjunctival hyperaemia, eyelash growth (hypertrichosis), increased iris and periorbital pigmentation, and deepening of the upper eyelid sulcus (DUES). Beta-adrenergic receptor antagonists (beta-blockers — timolol 0.25% or 0.5% twice daily; betaxolol 0.5% twice daily — cardioselective, safer in asthma): reduce aqueous production by 25–30%; contraindicated in asthma, COPD, heart block, and decompensated heart failure. Carbonic anhydrase inhibitors (CAIs — dorzolamide 2% twice or three times daily; brinzolamide 1% three times daily; oral acetazolamide 250–500 mg three to four times daily for acute angle-closure or pre-operative IOP control): reduce aqueous production. Alpha-2 agonists (brimonidine 0.15% or 0.2% twice daily): dual mechanism — reduces aqueous production and enhances uveoscleral outflow; also has neuroprotective properties in experimental models. Rho-kinase inhibitors (netarsudil 0.02% once nightly — Rhopressa): newest class; directly targets trabecular meshwork; reduces IOP 20–25%; causes conjunctival hyperaemia in 50%. Laser treatments: Selective laser trabeculoplasty (SLT): delivered at 532 nm to trabecular meshwork pigmented cells; reduces IOP by 25–30% in open-angle glaucoma; the LiGHT trial demonstrated SLT as effective as topical medication as primary treatment with better adherence and quality of life; repeatable once (partial effect recurs). Laser peripheral iridotomy (LPI): first-line treatment for angle-closure glaucoma — a small hole created in the peripheral iris with a Nd:YAG laser relieves relative pupil block and deepens the anterior chamber angle, preventing closure. Surgical treatment: trabeculectomy (partial-thickness guarded sclerectomy — creating a subconjunctival filtration bleb through which aqueous drains); Mitomycin-C (MMC) or 5-fluorouracil (5-FU) antimetabolite augmentation reduces scarring and improves bleb survival; trabeculectomy reduces IOP by 35–40% and is highly effective for advanced glaucoma. Minimally invasive glaucoma surgery (MIGS — iStent, Hydrus microstent, Xen gel stent): IOP reduction of 15–25%; lower risk profile than trabeculectomy; suitable for mild-to-moderate glaucoma, particularly combined with phacoemulsification cataract surgery.

The primary complication of untreated or inadequately treated glaucoma is progressive, irreversible visual field loss leading to blindness. Unlike many other causes of blindness, glaucomatous damage cannot be reversed — vision lost is permanent. Acute angle-closure glaucoma can cause permanent vision loss within hours if not treated emergently with IOP-lowering medications and laser peripheral iridotomy. Trabeculectomy carries surgical risks including infection (endophthalmitis), hypotony (excessively low IOP causing vision problems), and cataract formation. Glaucoma medication side effects include eye irritation, systemic beta-blocker effects (bradycardia, bronchospasm), and periorbital skin darkening with prostaglandins.

Regular comprehensive eye examinations every 1–2 years — including IOP measurement and optic disc assessment — from age 40 (or earlier for high-risk individuals) is the cornerstone of glaucoma prevention through early detection. Adhere strictly to prescribed eye drops and never stop medication without ophthalmology advice; even if vision seems unchanged, drops prevent ongoing silent damage. Avoid prolonged use of steroid eye drops or nasal sprays without ophthalmology monitoring, as steroids can raise IOP. Family members of glaucoma patients should have regular eye examinations given 10-fold increased risk. Angle-closure risk can be prevented with prophylactic laser peripheral iridotomy in susceptible eyes.

Go to A&E or an eye emergency department immediately for: sudden severe eye pain with headache, nausea, vomiting, and blurred vision with halos around lights — this is acute angle-closure glaucoma, a medical emergency where IOP can reach 50–70 mmHg within hours, causing irreversible blindness if not treated urgently with IV acetazolamide and laser iridotomy. See an ophthalmologist within 24–48 hours for: any new sudden loss of peripheral or central vision; sudden onset of multiple new floaters with flashes of light (possibly retinal tear — different emergency). Book a routine eye examination with an optometrist within 1–2 months if: you are over 40 and have not had an eye test including IOP measurement in the past 2 years; you have a first-degree relative with glaucoma (10-fold increased risk — annual eye tests are recommended); you are over 60, of Black African or Caribbean ancestry, have diabetes, severe myopia, or have been using steroid eye drops or nasal sprays for more than 6 weeks without ophthalmology monitoring. In the UK, glaucoma suspects and people over 40 with a parent or sibling with glaucoma are eligible for free NHS sight tests.