Open-angle glaucoma !
Open-angle glaucoma slowly damages the optic nerve, often with high eye pressure; it narrows side vision without pain and can lead to blindness.
Updated 2026-10-30
Structures involved
Tap one to see what it is and open it in 3D.
In histology
In the clinical exam
- Eye exam: visual acuity, visual fields and eye movements
- Fundoscopy: the optic disc, papilledema and retinopathy
In physiology
Why it happens
What it is
Chronic, progressive optic neuropathy in which retinal ganglion cell axons are lost, the optic disc becomes cupped and the visual field shrinks, with an open drainage angle. Raised intraocular pressure is its main modifiable risk factor.
Who gets it
A leading cause of irreversible blindness worldwide. Its prevalence rises steeply with age and is higher in people of African ancestry. Because it is silent, a large share of people with glaucoma do not know they have it. In Colombia's 2015 SABE survey of adults aged 60 or older, 5.67% reported a glaucoma diagnosis (any type), more often women.
Causes
- Primary: reduced aqueous outflow through the trabecular meshwork, cause not fully understood
- Normal-tension glaucoma: damage with pressures in the normal range
- Secondary open-angle forms: corticosteroid use, pigment dispersion, pseudoexfoliation, trauma, uveitis
Risk factors
- Raised intraocular pressure
- Older age
- African ancestry
- Family history of glaucoma
- Thin central cornea, myopia
- Long-term corticosteroids (drops, inhaled or systemic)
Pathophysiology
Aqueous humour made by the ciliary body leaves the eye through the trabecular meshwork at the drainage angle. Higher resistance raises intraocular pressure, which stresses ganglion cell axons where they pass through the optic disc. Axons die, the cup enlarges and the field is lost from the periphery inwards, while central acuity survives until late.
Symptoms and signs
- No symptoms in early and moderate disease
- No pain or redness
- Gradual loss of peripheral vision, usually unnoticed
- Late: tunnel vision, bumping into objects, then loss of central vision
Diagnosis
- Clinical
- Comprehensive eye examination: tonometry (applanation) for intraocular pressure, gonioscopy to confirm an open angle, and dilated optic disc examination for an increased cup-to-disc ratio, rim notching, asymmetry or disc haemorrhage.
- Tests
- Standard automated perimetry (visual fields) shows typical arcuate defects and nasal steps. Pachymetry measures corneal thickness, which affects the pressure reading.
- Imaging
- Optical coherence tomography (OCT) measures the retinal nerve fibre layer and ganglion cell layer; disc photographs document change over time.
Differential diagnosis
- Ocular hypertension (high pressure without nerve damage)
- Primary angle-closure glaucoma
- Physiologically large optic cup
- Compressive optic neuropathy (pituitary or other tumour)
- Ischaemic optic neuropathy
- Retinal disease causing field loss
Goal of treatment
Lower intraocular pressure to a target that stops or slows further nerve damage, preserving the remaining vision for life. Lost vision cannot be restored.
Treatment
- Medical
- Pressure-lowering eye drops: prostaglandin analogues (often first line), beta-blockers, alpha-2 agonists, carbonic anhydrase inhibitors and rho-kinase inhibitors, alone or combined.
- Procedure
- Laser trabeculoplasty (selective) improves trabecular outflow and is an accepted first-line alternative to drops.
- Surgical
- Trabeculectomy, glaucoma drainage devices or minimally invasive glaucoma surgery when pressure is not controlled or the disease progresses.
- Follow-up
- Lifelong follow-up with pressure checks, visual fields and OCT; adherence to drops is a key challenge.
Drugs for this condition
Complications
- Irreversible visual field loss and blindness
- Systemic effects of topical beta-blockers (bronchospasm, bradycardia)
- Ocular surface irritation from long-term drops
- Surgical: hypotony, infection of the filtering bleb, cataract
Prognosis
With early detection and sustained pressure control most people keep useful vision for life. Late diagnosis, poor adherence and very high pressure lead to progression and blindness.
Prevention
- Regular eye examinations from middle age, earlier for people with a family history, African ancestry, high myopia or long-term corticosteroids; screening intervals vary between guidelines
- Examining first-degree relatives of patients
Test yourself
Think of the answer, then tap the question to see it.
Why is primary open-angle glaucoma called the «silent thief of sight»?
It is painless and peripheral vision is lost gradually, so most people notice nothing until damage is advanced.
What optic disc sign is characteristic of glaucoma?
An increased cup-to-disc ratio (cupping), with rim thinning or notching and asymmetry between the eyes.
What is the main modifiable risk factor for open-angle glaucoma?
Raised intraocular pressure; lowering it is the only proven treatment.
Which drug class is often first line for open-angle glaucoma?
Topical prostaglandin analogues, which increase uveoscleral outflow.
Which examination distinguishes open-angle from angle-closure glaucoma?
Gonioscopy, which shows whether the drainage angle is open.
Related conditions
- Cataract
- Type 2 diabetes mellitus
- Acute angle-closure glaucoma
- Diabetic retinopathy
- Age-related macular degeneration
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Open Angle Glaucoma (StatPearls (NCBI Bookshelf), 2024); Self-reported glaucoma prevalence and related factors, contribution to reported visual impairment, and functional burden in a cross-sectional study in Colombia (International ophthalmology, 2023) · adapted, CC BY 4.0.
Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake
Representative model, for educational purposes only.
