Glaucoma

Glaucoma is a group of progressive optic neuropathies characterised by retinal ganglion cell loss and characteristic optic disc changes, with raised intraocular pressure being the most important modifiable risk factor.

PLAB 1UKMLA1 questions

Key Facts

Glaucoma is the leading cause of irreversible blindness worldwide; affects approximately 700,000 people in the UK Primary open-angle glaucoma (POAG) accounts for ~90% of cases; chronic, progressive, initially asymptomatic Intraocular pressure (IOP) is the main modifiable risk factor; normal range 10-21mmHg; but normal-tension glaucoma occurs with IOP ≤21 NICE NG81: first-line treatment is a prostaglandin analogue (latanoprost 0.005% drops OD at night) Visual field loss: starts as arcuate scotoma (nasal step); central vision preserved until late; "tunnel vision" in advanced disease Optic disc changes: increased cup-to-disc ratio (>0.7), asymmetry between eyes (>0.2 difference), disc haemorrhage, nerve fibre layer defects Risk factors: age >40, African-Caribbean ethnicity (4× risk), family history (10× in first-degree relatives), myopia, thin central cornea Screening: not a national programme; opportunistic detection through optometrist IOP and disc assessment

Overview

Key Facts

Glaucoma is often called the "silent thief of sight" because it is typically asymptomatic until significant irreversible visual field loss has occurred. Early detection and treatment are essential.

Epidemiology

  • ~700,000 affected in the UK; ~2% of >40s
  • Leading cause of irreversible blindness worldwide
  • 50% of cases remain undiagnosed
  • Prevalence increases with age: 1% at 40, 5% at 80

Aetiology

  • Primary open-angle glaucoma (POAG): open drainage angle; impaired trabecular meshwork outflow
  • Primary angle-closure glaucoma (PACG): anatomically narrow angle; see separate topic for acute angle-closure
  • Secondary: steroid-induced, uveitic, neovascular (proliferative diabetic retinopathy), pseudoexfoliation, pigment dispersion
  • Congenital/developmental: rare; present in infancy with buphthalmos

Pathophysiology

  • IOP determined by aqueous humour production (ciliary body) and drainage (trabecular meshwork → canal of Schlemm; or uveoscleral outflow)
  • In POAG: increased resistance to outflow through trabecular meshwork
  • Elevated IOP → mechanical compression of retinal ganglion cell axons at the lamina cribrosa → progressive axonal loss → optic disc cupping → visual field loss
  • Vascular factors (reduced optic disc perfusion) also contribute, especially in normal-tension glaucoma

Clinical Presentation

POAG

  • Asymptomatic until advanced (peripheral vision lost first; central preserved until late)
  • Detected at routine optometry: raised IOP, suspicious disc, field defect
  • Bilateral but often asymmetric
  • No pain or redness

Symptoms of Advanced Disease

  • Tunnel vision
  • Difficulty with mobility (bumping into things)
  • Near-misses (driving)
  • Eventually total blindness if untreated

Red Flags

  • Rapid visual field loss (suspect secondary cause or poor compliance)
  • Young patient with glaucoma (consider secondary causes, congenital)
  • Unilateral raised IOP with inflammation (uveitic glaucoma)
  • IOP >40mmHg (acute angle-closure or secondary cause)

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Ocular hypertensionRaised IOP, normal disc and fieldsMonitoring
Normal-tension glaucomaNormal IOP, disc changes, field loss24h IOP profile, neuroimaging
Physiological cuppingLarge cup, no progression, normal fieldsSerial monitoring
Optic disc drusenPseudopapilloedema, autofluorescenceB-scan USS, OCT
Compressive optic neuropathyDisc pallor, RAPD, field defectMRI brain/orbits
Secondary glaucomaSteroid use, uveitis, neovascularisationClinical context

Diagnosis / Investigation

Bedside

  • Visual acuity
  • IOP measurement: Goldmann applanation tonometry (gold standard); normal 10-21mmHg
  • Gonioscopy: angle assessment (open vs closed)

Bloods

  • Not routinely needed

Imaging

  • OCT (optical coherence tomography): retinal nerve fibre layer (RNFL) thickness; detects early damage before visual field loss
  • Visual field testing (Humphrey/standard automated perimetry): detects arcuate scotoma, nasal step
  • Optic disc photography: baseline and serial monitoring

Special Tests

  • Central corneal thickness (CCT): thin cornea (≤555μm) underestimates true IOP and is an independent risk factor
  • Disc assessment: cup-to-disc ratio (CDR), neuroretinal rim, disc haemorrhage, RNFL defects
  • 24-hour IOP profile: for normal-tension glaucoma
  • Repeat visual fields for confirmation (learning effect in first test)

Management

Non-pharmacological

  • Patient education about chronic nature and importance of adherence
  • Driving standards (DVLA): must have adequate binocular visual field

Pharmacological (NICE NG81)

  • First-line: prostaglandin analogue — latanoprost 0.005% drops OD at night
    • Side effects: eyelash growth, iris pigmentation (permanent), periorbital fat atrophy
    • Alternatives: bimatoprost, travoprost, tafluprost
  • Second-line (if PGA insufficient/not tolerated): add or switch to:
    • Beta-blocker: timolol 0.5% BD (avoid in asthma, heart block, bradycardia)
    • Carbonic anhydrase inhibitor: dorzolamide 2% TDS or brinzolamide 1% BD
    • Alpha-2 agonist: brimonidine 0.2% BD
  • Combination drops: available for adherence (e.g. Cosopt = timolol + dorzolamide; Ganfort = bimatoprost + timolol)
  • Maximum medical therapy: combination of 2-3 agents from different classes

Surgical/Interventional

  • Selective laser trabeculoplasty (SLT): can be first-line alternative to drops (LiGHT trial); well-tolerated; repeatable
  • Trabeculectomy: gold standard surgical treatment for uncontrolled glaucoma; creates fistula for aqueous drainage
  • Tube shunt/drainage device: for complex or refractory glaucoma
  • Minimally invasive glaucoma surgery (MIGS): iStent, trabectome; for mild-moderate glaucoma (often combined with cataract surgery)
  • Cyclophotocoagulation: for refractory end-stage glaucoma

Referral Criteria

  • Raised IOP with suspicious disc or field defect: urgent ophthalmology referral
  • Established glaucoma: lifelong ophthalmology follow-up
  • Rapidly progressing: specialist glaucoma service

Prognosis

  • POAG is a lifelong condition; treatment slows but does not reverse damage
  • Treatment reduces IOP by 25-30% and significantly reduces visual field loss progression
  • LiGHT trial: SLT as effective as drops for first-line IOP reduction
  • Untreated: progressive bilateral visual field loss → tunnel vision → blindness
  • Normal-tension glaucoma: treatment still beneficial (CNTGS trial: 30% IOP reduction slowed progression)
  • CVI registration: approximately 10% of glaucoma patients become registered sight impaired
  • Adherence is a major challenge (50% non-adherent at 1 year)

Other Relevant Information

NICE NG81 — Treatment Pathway

StepTreatment
1Prostaglandin analogue (latanoprost) OR SLT
2Add beta-blocker (timolol) or switch class
3Add CAI (dorzolamide) or alpha-agonist (brimonidine)
4Maximum medical therapy
5Trabeculectomy or tube shunt

Types of Glaucoma

TypeAngleIOPOnset
POAGOpenUsually raisedChronic, insidious
Normal-tensionOpenNormalChronic
Acute angle-closureClosedVery highAcute emergency
SecondaryVariableRaisedDepends on cause