Glaucoma — Causes, Types, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Glaucoma is a group of progressive optic neuropathies characterised by characteristic structural damage to the optic nerve head (optic disc cupping — loss of neuroretinal rim tissue) and corresponding visual field loss, typically associated with elevated intraocular pressure (IOP). It is the leading cause of irreversible blindness globally, affecting approximately 80 million people — with half unaware of their diagnosis due to its insidious, asymptomatic course in the most common form. Primary open-angle glaucoma (POAG) accounts for 74% of all glaucoma — a chronic, slowly progressive condition in which the trabecular meshwork drainage angle remains open but aqueous outflow is impaired. Normal-tension glaucoma (NTG) — optic nerve damage despite IOP within the statistical normal range (10-21 mmHg) — accounts for 30% of POAG. Acute angle-closure glaucoma (AACG) is a medical emergency characterised by sudden, severe IOP elevation from blocked aqueous outflow, causing acute painful vision loss.

Elevated IOP is the primary modifiable risk factor — aqueous humour is produced by the ciliary body and drains through the trabecular meshwork into Schlemm's canal; impaired drainage elevates IOP. Each 1 mmHg reduction in IOP reduces glaucoma progression risk by approximately 10%. Primary open-angle glaucoma (POAG) risk factors: elevated IOP (IOP above 21 mmHg — ocular hypertension); advancing age (prevalence doubles each decade over 40); Black ethnicity (5x higher risk — more severe and earlier onset); family history of POAG (first-degree relative — risk 4-9x); high myopia (axial elongation strains optic nerve); central corneal thickness below 555 mcm (thin cornea — underestimates true IOP). Angle-closure glaucoma risk factors: Asian ethnicity (significantly higher anatomical predisposition); female sex; hypermetropia (far-sightedness — shorter eye length pushes iris forward); advancing age (lens thickening narrows drainage angle); family history. Secondary glaucoma causes: exfoliation syndrome (exfoliative material clogs trabecular meshwork — most common secondary cause worldwide); pigment dispersion syndrome; uveitis; neovascular glaucoma (from diabetic retinopathy, CRVO); steroid-induced glaucoma (topical, periocular, systemic, or inhaled corticosteroids); trauma; and previous intraocular surgery. Genetics: MYOC (myocilin gene) mutations cause 4% of POAG; OPTN and TBK1 (normal-tension glaucoma).

Primary open-angle glaucoma is typically completely asymptomatic until very advanced — the peripheral visual field is lost first (superior nasal arcuate visual field loss), which the brain suppresses without the patient noticing. By the time vision loss becomes subjectively apparent (central vision affected), 90% of optic nerve fibres may already be irreversibly damaged. This is why opportunistic detection through routine eye examinations is critical. Acute angle-closure glaucoma (AACG) — a true ocular emergency — presents dramatically: sudden severe pain around the eye and orbit; red eye (ciliary flush); markedly reduced vision and coloured halos around lights; nausea and vomiting (vagal response to severe pain); steamy (hazy) cornea from corneal oedema; fixed mid-dilated pupil (approximately 4-5 mm, oval, non-reactive to light). IOP in AACG typically exceeds 40-50 mmHg (normal 10-21 mmHg) and requires immediate treatment to prevent permanent optic nerve damage. Chronic angle closure: similar to POAG but may include intermittent episodes of mild pain, blurred vision, and haloes (sub-acute attacks).

NICE recommends referral to ophthalmology for any suspicion of glaucoma (IOP above 24 mmHg, suspicious disc, or visual field defect). Comprehensive glaucoma assessment: tonometry — non-contact (air puff) or Goldmann applanation tonometry (gold standard) measures IOP; central corneal thickness (CCT) by pachymetry (thin cornea underestimates true IOP; thick cornea overestimates). Optic disc assessment: slit-lamp biomicroscopy with +90D or +78D lens; optic disc photography; assessment of cup-to-disc ratio (CDR — above 0.7 or asymmetric CDR is suspicious); neuroretinal rim thinning (especially inferior and superior poles — ISNT rule). Optical coherence tomography (OCT): measures retinal nerve fibre layer (RNFL) thickness and ganglion cell complex — detects structural optic nerve damage earlier than visual field testing. Visual field testing: automated threshold perimetry (Humphrey Visual Field Analyser 24-2 or 30-2) — detects and tracks functional glaucomatous field loss (arcuate scotoma, nasal step, temporal wedge defect); reliable results require patient cooperation. Gonioscopy: direct visualisation of the trabecular drainage angle — essential to classify open vs. closed angle. Ultrasound biomicroscopy or anterior segment OCT: imaging the angle in suspected angle closure.

All current glaucoma treatments aim to lower IOP — the only proven modifiable factor. Target IOP is individualised: typically 25-30% reduction from baseline, or below 18 mmHg in early POAG; more aggressive reduction in advanced disease or NTG. Medical (eye drops): prostaglandin analogues — latanoprost 0.005% once nightly (first-line, NICE recommended — most effective class: reduces IOP by 25-35%; increases uveoscleral outflow); bimatoprost, travoprost, tafluprost. Beta-blockers — timolol 0.5% BD (do not use in asthma, COPD, or heart block); carbonic anhydrase inhibitors — dorzolamide, brinzolamide (topical), acetazolamide (oral — for acute angle closure); alpha-agonists — brimonidine 0.2% (neuroprotective effect also suggested). Fixed combinations (latanoprost/timolol, dorzolamide/timolol) improve adherence. Laser treatment: selective laser trabeculoplasty (SLT) — non-invasive, repeatable laser to trabecular meshwork stimulating macrophage activity and improving aqueous drainage; reduces IOP by 20-30%; LiGHT trial (2019) shows SLT is superior to drops as first-line for POAG and OHT; laser peripheral iridotomy (LPI) — first-line for angle closure and acute angle-closure crisis — creates hole in peripheral iris allowing aqueous bypass. Surgery: trabeculectomy (filtering surgery — creates new drainage pathway; gold standard for advanced glaucoma; reduces IOP by 30-40%); glaucoma drainage devices (Ahmed, Baerveldt — for refractory cases); minimally invasive glaucoma surgery (MIGS — iStent, Hydrus, Xen gel stent — suitable for mild-moderate glaucoma combined with cataract surgery). Acute angle closure emergency treatment: IV acetazolamide 500 mg; IV mannitol; topical pilocarpine; intensive topical anti-glaucoma drops; supine positioning for posterior pupillary block; followed by urgent LPI when cornea clears.

Irreversible optic nerve damage and progressive visual field loss are the defining complications of glaucoma — lost peripheral vision cannot be restored, even with effective IOP control. Untreated or inadequately managed glaucoma progresses to blindness; it is the leading cause of irreversible blindness globally. Peripheral visual field loss below DVLA standards (binocular Esterman field below 120 degrees horizontal) legally requires cessation of driving — a major impact on independence. Falls and hip fractures are significantly more common in patients with peripheral visual field defects — inferior field loss from superior arcuate scotoma creates particular hazard on stairs and uneven ground. Neovascular glaucoma from diabetic retinopathy or central retinal vein occlusion causes refractory raised IOP with severe pain and rapid visual loss — often progresses to blindness despite maximal treatment. Trabeculectomy surgical complications include hypotony (over-filtration causing choroidal detachment), bleb infection (blebitis), and delayed endophthalmitis. Psychological impact of diagnosed glaucoma — anxiety about blindness and treatment burden affects approximately 30-40% of patients.

Glaucoma cannot be prevented, but blindness from glaucoma is largely preventable through early detection and treatment. Regular optometric eye examinations: every 2 years (every 1 year if risk factors — family history, Black ethnicity, myopia) — optometrists perform IOP measurement and optic disc assessment as part of standard eye test; referral to ophthalmology if suspicious. NHS England funds free NHS sight tests for: those over 60; those over 40 with a first-degree family history of glaucoma. Ocular hypertension treatment: latanoprost drops or SLT for IOP above 24 mmHg with risk factors significantly reduces conversion to POAG (Ocular Hypertension Treatment Study — 50% risk reduction). Avoid prolonged topical, periocular, or inhaled corticosteroid use without monitoring IOP (steroid response glaucoma). Inform glaucoma patients: stop driving if binocular visual field fails DVLA standard; glaucoma is registrable visual impairment if severe.

Go to Emergency Department immediately for: sudden severe eye pain with reduced vision and red eye — acute angle-closure glaucoma is an ocular emergency; delay causes permanent optic nerve damage and blindness within hours. Features: severe throbbing orbital pain, nausea, reduced vision, coloured halos around lights, steamy cornea, fixed mid-dilated pupil. Also attend urgently for: sudden painless visual field loss or vision loss with no obvious cause (may indicate other serious eye conditions alongside glaucoma). Book urgent optometry or ophthalmology appointment if: a first-degree relative has been diagnosed with glaucoma (you need baseline IOP and disc assessment); you notice gradual loss of peripheral vision or increased difficulty with night driving. Glaucoma progression requires lifelong ophthalmology monitoring — never stop eye drops without specialist advice; poor adherence is the main cause of avoidable glaucoma blindness.