Chronic Open-Angle Glaucoma
Chronic open-angle glaucoma is a chronic optic neuropathy characterised by progressive optic disc changes and visual field defects, despite an open iridocorneal angle. It is commonly associated with raised intraocular pressure, although normal-tension glaucoma can also occur.
This updated UKMLA guide to chronic open-angle glaucoma is based on NICE NG81 and NICE CKS, which covers causes, risk factors, symptoms, diagnosis, and management.
Terms and Definitions
| Term / condition | Definition / description |
|---|---|
| Glaucoma | A group of eye diseases that cause progressive optic neuropathy, characterised by visual field defects and optic disc changes
Commonly associated with raised IOP |
| Ocular hypertension | Elevated IOP (> 21 mmHg) but with no signs of glaucoma (i.e. no optic neuropathy / no visual field defect) |
| Normal tension glaucoma | Presence of optic neuropathy (characterised by visual field defects and optic disc changes), but with normal IOP |
| Angle-closure glaucoma (narrow-angle glaucoma) | Glaucoma secondary to narrowing/closure of the iridocorneal angle → impaired aqueous humour drainage → ↑ IOP
Most often presents acutely |
| Open-angle glaucoma | Glaucoma secondary to trabecular meshwork dysfunction, despite an open (normal) iridocorneal angle
Often associated with ↑ IOP Most often presents chronically |
Raised IOP ≠ glaucoma.
Optic nerve neuropathy is needed for it to be glaucoma, indicated by optic disc changes and visual-field defects.
Relevant Anatomy and Physiology
Intra-ocular pressure (IOP)
- IOP helps maintain the shape of the globe
- IOP is mainly determined by the balance between aqueous humour production and aqueous humour drainage
Aqueous humour pathway:
- Produced by the ciliary body (the enzyme carbonic anhydrase plays an important role)
- Flows from the posterior chamber, through the pupil, into the anterior chamber
- Drained out of the eye via the iridocorneal angle → trabecular meshwork → Schlemm’s canal
- A small % is drained via the uveoscleral pathway (via the venous circulation of the iris, ciliary body, choroid, and sclera)
Control of aqueous humour secretion:
- Stimulated by beta-2 receptors
- Decreased by alpha-2 receptors
Causes
Open-angle glaucoma is most commonly primary (POAG):
- POAG is the most common type of glaucoma overall
- It is thought to result from trabecular meshwork dysfunction → impaired aqueous humour drainage despite a normal (open) iridocorneal angle → raised IOP → progressive optic nerve damage
Risk Factors
Key risk factors:
- Raised IOP – major risk factor (~10% of patients with raised IOP develop glaucoma after 5 years; 30% after 20 years)
- Advancing age
- Family history and genetic variants (most common gene: MYOC)
- Black people
- Use of corticosteroids (oral / inhaled / high-potency topical) – exact mechanism unclear but likely to change the stiffness of the trabecular network
- Myopia (short-sighted)
Normal tension glaucoma occurs in a significant minority of people with POAG, where glaucoma develops with normal IOP.
Hypermetropia (long-sighted) → shorter eye axis → associated with angle-closure glaucoma
Myopia (short-sighted) → longer eye axis → associated with open-angle glaucoma
Diagnosis
Clinical Features
Primary open-angle glaucoma is usually insidious in onset and follows a chronic course
- Often asymptomatic
- Visual impairment / visual field defect
- Typically bilateral and progressive
- First affects peripheral vision (tunnel vision), then central vision
Investigation and Diagnosis
Raised IOP ≠ glaucoma.
Optic nerve neuropathy is needed for it to be glaucoma, indicated by 1) optic disc changes and 2) visual-field defects.
Key tests and interpretation: [Ref1][Ref2]
| Test / investigation | Findings in primary open-angle glaucoma |
|---|---|
| Fundoscopy | The following finding suggest optic neuropathy:
|
| Visual field assessment (with automated perimetry) | First affects peripheral vision (tunnel vision), then central vision
Classic visual field defect patterns:
|
| IOP measurement with tonometry | Gold standard: Goldmann applanation tonometer
The central corneal thickness should be measured, as a thin cornea underestimates true IOP, and a thick cornea overestimates IOP. |
| Slit lamp examination (with pupil dilation) | Slit lamp examination should involve:
|
| Other investigation | OCT or optic nerve head imaging can also be used to assess for optic neuropathy |
To diagnose primary open-angle glaucoma, there should be:
- Open (normal) iridocorneal angle – demonstrated on gonioscopy, AND
- Evidence of optic neuropathy, indicated by
- Visual field defect
- Optic disc changes (e.g. cupping)
Raised IOP is often present and is the most important modifiable risk factor, but it is not required for diagnosis.
NICE Recommendations
Offer ALL the following tests before referral (for primary eye care professionals):
- Central visual field assessment using automated perimetry
- IOP measurement with Goldmann applanation tonometer
- Optic nerve assessment and fundus examination with stereoscopic slit lamp biomicroscopy and OCT or optic nerve head image
- Peripheral anterior chamber configuration and depth assessment with gonioscopy / van Herick test / OCT
After the above tests, refer to ophthalmology if ANY of the following are present:
- IOP ≥24 mmHg (only if measured with Goldmann-type applanation tonometry)
- Visual field defect
- Optic nerve head damage
In secondary care, offer ALL the following tests:
- Central visual field assessment using automated perimetry
- IOP measurement with Goldmann-type applanation tonometry (slit lamp mounted)
- Optic nerve assessment and fundus examination with stereoscopic slit lamp biomicroscopy with pupil dilatation
- Peripheral anterior chamber configuration and depth assessment with gonioscopy
- Central corneal thickness measurement
Management
Ocular Hypertension (OHT)
Indications to treat:
- IOP ≥24 mmHg, PLUS
- The patient is at risk of visual impairment within their lifetime (e.g. thin cornea thickness, +ve family history, life expectancy long enough for OHT to progress into glaucoma)
Initial Treatment
1st line: 360° selective laser trabeculoplasty (SLT)
- SLT may delay the need for eye drops, but does NOT remove the chance they will be needed at all
- Consider a second attempt if the initial successful SLT has reduced over time
Offer a generic prostaglandin analogue (e.g. latanoprost, travoprost, tafluprost, bimatoprost), if:
- Patient wishes to avoid SLT
- SLT is not suitable (e.g. pigment dispersion syndrome)
- Patient is waiting for SLT and needs interim treatment
Ongoing Pharmacological Management
If SLT did NOT reduce IOP sufficiently (e.g. >24 mmHg), start topical medications:
- 1st line: generic prostaglandin analogue (e.g. latanoprost, travoprost, tafluprost, bimatoprost)
- If still insufficient, check adherence and eye drop technique first, then add other drug classes:
- Beta-blocker (e.g. timolol, levobunolol, betaxolol)
- Carbonic anhydrase inhibitor (e.g. dorzolamide, brinzolamide)
- Sympathomimetic (e.g. brimonidine)
If the current treatment is not tolerated, consider an alternative treatment in the following order:
- 1st line: alternative generic prostaglandin analogue (e.g. latanoprost, travoprost, tafluprost, bimatoprost)
- 2nd line: beta-blocker (e.g. timolol, levobunolol, betaxolol)
- 3rd line: non-generic prostaglandin analogue / carbonic anhydrase inhibitor (e.g. dorzolamide, brinzolamide) / sympathomimetic (e.g. brimonidine) / miotics (e.g. pilocarpine hydrochloride)/ combination of treatments
Chronic Open-Angle Glaucoma (COAG)
Consider treatment if: IOP ≥24 mmHg OR at risk of visual impairment within their lifetime (e.g. thin cornea thickness, +ve family history, life expectancy long enough for OHT to progress into glaucoma)
Non-Advanced COAG
1st line: 360° selective laser trabeculoplasty (SLT)
- SLT may delay the need for eye drops, but does NOT remove the chance they will be needed at all
- Consider a second attempt if the initial successful SLT has reduced over time
Offer a generic prostaglandin analogue (e.g. latanoprost, travoprost, tafluprost, bimatoprost), if:
- Patient wishes to avoid SLT
- SLT is not suitable (e.g. pigment dispersion syndrome)
- Patient is waiting for SLT and needs interim treatment
If SLT did NOT reduce IOP sufficiently (e.g. >24 mmHg) or there is progression in optic nerve head damage / visual field defect → start generic prostaglandin analogue (e.g. latanoprost, travoprost, tafluprost, bimatoprost)
If still insufficient, check adherence and eye drop technique first, then offer ONE of the following:
- Add another drug class (usually considered first)
- Beta-blocker (e.g. timolol, levobunolol, betaxolol)
- Carbonic anhydrase inhibitor (e.g. dorzolamide, brinzolamide)
- Sympathomimetic (e.g. brimonidine)
- 360° selective laser trabeculoplasty (SLT)
- Glaucoma surgery with (e.g. surgical trabeculectomy) with mitomycin-C
Consider 360° SLT or glaucoma surgery with mitomycin-C for those who are at risk of progressing to sight loss despite treatment with medicines from 2 therapeutic classes.
Cyclodiode laser treatment is an option for further therapy (e.g. glaucoma surgery ineffective or not appropriate)
Advanced COAG
Offer:
- Glaucoma surgery (e.g., surgical trabeculectomy), AND
- Pharmacological augmentation with mitomycin-C
Monitoring and Reassessment
At each assessment:
- Measure IOP with Goldmann applanation tonometry (slit lamp mounted)
- Anterior segment slit lamp examination
If clinically indicated, also offer:
- Repeat gonioscopy
- Repeat visual field testing with automated perimetry
- Repeat assessment of the optic nerve head