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Glaucoma

SNOMED: 23986001998 wordsUpdated 03/03/2026
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Exam Tips

  • Do not exclude glaucoma because IOP is normal; normal-tension glaucoma is common in exams and clinics.
  • Primary open-angle glaucoma is classically silent early; ask specifically about peripheral vision and driving difficulties.
  • Acute angle closure is an ophthalmic emergency: painful red eye + haloes + nausea/vomiting + mid-dilated pupil.
  • Differentiate OHT, suspected glaucoma, and definite glaucoma by combining optic disc, visual field, and IOP findings.
  • First-degree family history and steroid exposure are high-yield risk factors in OSCE history stations.
  • In management questions, include contraindications to topical timolol (asthma, bradyarrhythmia/heart block).

Definition

Glaucoma is a group of chronic, progressive optic neuropathies in which retinal ganglion cell loss causes characteristic optic disc cupping and corresponding visual field loss. Intraocular pressure (IOP) is the main modifiable risk factor, but damage can occur at statistically normal pressures (normal-tension glaucoma), so diagnosis depends on structure and function, not IOP alone.

Pathophysiology

Aqueous humour is produced by the ciliary epithelium (carbonic anhydrase-dependent), passes from posterior chamber through the pupil, and drains mainly via trabecular meshwork/Schlemm canal with a smaller uveoscleral pathway. IOP reflects balance between production and outflow; impaired outflow (most commonly at trabecular meshwork in open-angle disease, or mechanical angle obstruction by peripheral iris in angle-closure disease) raises IOP and increases trans-laminar stress at the optic nerve head. This leads to retinal ganglion cell axonal injury, neuroretinal rim thinning, and progressive arcuate/peripheral field defects; vascular dysregulation/ischemia also contributes, especially in normal-tension glaucoma. Secondary mechanisms include pseudoexfoliative material, pigment, neovascular membranes, inflammation, trauma (angle recession), and corticosteroid-induced outflow resistance. See Figure: anterior chamber angle and aqueous flow pathway (anatomy diagram commonly used in ophthalmology texts/AAO resources).

Risk Factors

  • Raised IOP (most important treatable risk factor)
  • Increasing age (risk rises markedly after 40 years)
  • Family history in first-degree relatives (higher risk, especially siblings)
  • Black ethnicity for primary open-angle glaucoma
  • East Asian/Chinese ethnicity for primary angle-closure glaucoma
  • Myopia (open-angle risk); hyperopia/short axial length (angle-closure risk)
  • Female sex (angle-closure risk)
  • Corticosteroid exposure (topical ocular, inhaled, oral, topical skin, IV)
  • Type 2 diabetes, hypertension, cardiovascular disease
  • Obstructive sleep apnoea

Clinical Features

Symptoms

  • Primary open-angle glaucoma is often asymptomatic until late disease
  • Gradual peripheral visual loss (difficulty with mobility/driving), later tunnel vision
  • Late central visual impairment (reading difficulty)
  • Acute angle closure: sudden severe unilateral eye pain, blurred vision/haloes, headache, nausea and vomiting
  • Subacute/intermittent angle closure: transient episodes of blur, haloes, ocular discomfort

Signs

  • Raised IOP (though may be normal in normal-tension glaucoma)
  • Optic disc cupping with increased cup-to-disc ratio, focal notch, disc haemorrhage
  • Corresponding visual field defects (nasal step, arcuate scotoma, paracentral defects)
  • Acute angle closure: red painful eye, corneal oedema, mid-dilated fixed pupil, shallow anterior chamber
  • Gonioscopy: open angle in POAG, narrow/closed angle in angle-closure spectrum

Investigations

Goldmann applanation tonometry:IOP may be >21 mmHg in many cases, but can be normal in normal-tension glaucoma
Gonioscopy:Differentiates open-angle from narrow/closed-angle mechanisms
Dilated optic nerve head assessment (slit lamp + fundus exam):Pathological cupping, neuroretinal rim thinning/notching, possible disc haemorrhage
Automated perimetry (visual fields):Reproducible glaucomatous defects, often peripheral first
Optical coherence tomography (OCT) RNFL/GCC:Retinal nerve fibre layer and ganglion cell complex thinning
Central corneal thickness (pachymetry):Thin cornea increases risk/progression and affects IOP interpretation
Anterior segment examination:May show pseudoexfoliative material, pigment dispersion, uveitis, neovascularisation, or trauma signs in secondary glaucoma

Management

Lifestyle Modifications

  • Emphasise adherence to drops and follow-up (progression is often silent)
  • Review steroid use and minimise/stop if clinically safe
  • Advise urgent same-day assessment for any sudden painful red eye with visual symptoms
  • Discuss driving implications if visual fields are affected (DVLA standards)

Pharmacological Treatment

Prostaglandin analogue (first-line for many with OHT/POAG)

  • Latanoprost 50 micrograms/mL eye drops: 1 drop into affected eye(s) once nightly
  • Bimatoprost 300 micrograms/mL eye drops: 1 drop once nightly
  • Travoprost 40 micrograms/mL eye drops: 1 drop once nightly

Increase uveoscleral outflow; local adverse effects include conjunctival hyperaemia, eyelash growth, periocular skin darkening, and permanent iris pigmentation change; caution in active uveitis or herpetic keratitis history.

Topical beta-blocker

  • Timolol 0.25% to 0.5% eye drops: 1 drop once or twice daily
  • Betaxolol 0.25% to 0.5% eye drops: usually 1 drop twice daily

Reduce aqueous production; contraindicated in asthma/COPD with bronchospasm, sinus bradycardia, second/third-degree heart block, and uncontrolled heart failure; use punctal occlusion to reduce systemic absorption.

Topical carbonic anhydrase inhibitor

  • Dorzolamide 20 mg/mL eye drops: 1 drop two to three times daily
  • Brinzolamide 10 mg/mL eye drops: 1 drop twice daily

Reduce aqueous production; caution in severe renal impairment and sulfonamide hypersensitivity; may cause bitter taste and local irritation.

Alpha-2 agonist

  • Brimonidine 2 mg/mL eye drops: 1 drop two to three times daily

Reduces production and increases uveoscleral outflow; adverse effects include dry mouth, fatigue, allergic follicular conjunctivitis; avoid with MAOIs and use caution with TCAs; not for infants/very young children due to CNS depression risk.

Miotic (mainly angle-closure pathway once IOP starts to fall)

  • Pilocarpine 1% to 4% eye drops: typically 1 drop up to four times daily (specialist-directed)

Facilitates angle opening in pupillary block; less effective when IOP is extremely high due to ischaemic iris sphincter; can cause brow ache and induced myopia.

Systemic carbonic anhydrase inhibitor (acute pressure lowering)

  • Acetazolamide 500 mg immediate dose (oral or IV), then 250 mg four times daily short-term if needed

Used urgently in acute angle closure or severe pressure spikes; contraindications/cautions include sulfonamide allergy, severe renal/hepatic disease, hyponatraemia/hypokalaemia, adrenal insufficiency, and pregnancy considerations.

Surgical / Interventional

  • Selective laser trabeculoplasty (SLT) for open-angle glaucoma/ocular hypertension
  • Laser peripheral iridotomy (LPI) for primary angle closure/acute angle closure and often prophylaxis to fellow eye
  • Trabeculectomy with antimetabolite (e. g, mitomycin C) when target IOP not achieved medically/with laser
  • Glaucoma drainage devices (tube shunts) for refractory disease
  • Minimally invasive glaucoma surgery (MIGS) in selected patients, often with cataract surgery
  • Lens extraction in selected angle-closure anatomy

Complications

  • Progressive irreversible visual field loss
  • Tunnel vision and impaired mobility/driving
  • Central vision loss in advanced disease
  • Bilateral visual disability or blindness (minority, but significant burden)
  • Acute angle closure can cause rapid permanent optic nerve damage if treatment is delayed
  • Treatment-related adverse effects (ocular surface disease, systemic beta-blockade effects, post-surgical hypotony/infection/bleb leak)

Prognosis

Untreated glaucoma usually progresses, often slowly in POAG but variably between patients; many remain asymptomatic until substantial nerve fibre loss has occurred. With risk-stratified monitoring and timely IOP-lowering treatment, progression risk is significantly reduced, although existing visual loss is not reversible. In POAG, most patients do not become bilaterally blind, but a clinically important minority do, particularly with late presentation or poor control.

Sources & References

💊BNF Drug References(19)

NICE Guidelines(1)

📖Textbook References(2)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1095, 1096)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1096)[context]

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