Glaucoma (chronic open angle) (COAG)

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Aetiology

Chronic Open Angle Glaucoma (COAG) is a progressive optic neuropathy associated with a loss of retinal ganglion cells and their axons. The anterior chamber angle is open and there is no secondary cause for the optic nerve damage, e.g. steroid glaucoma, pseudoexfoliative or pigmentary glaucoma.
Affects approximately 2% of the white population of the UK aged over 40 years, increasing to 4-5% in the over-80s. Higher prevalence and greater severity in black ethnic groups.
Second most common cause of irreversible blindness in the UK (approx. 10% of certifiable severe sight impairment)
Incidence: M = F

Predisposing factors

Ocular hypertension
Increasing age
Positive family history in a first degree relative
People of West African descent including African-Caribbean; onset at younger age
Myopia
Type 2 diabetes mellitus
Low diastolic blood pressure and other vascular risk factors e.g. Raynauds disease

Symptoms of primary open angle glaucoma

Usually asymptomatic until there is significant loss of visual field

Signs of primary open angle glaucoma

Optic disc:

  • cupping:
    • generalised thinning, focal narrowing or notching of neuroretinal rim
    • cupping should be considered in relation to disc size
    • CD ratio >0.6 in average or smaller sized discs
    • R:L asymmetry (CD ratio ≥ 0.2 in similarly sized discs)
  • the disc damage likelihood scale (DDLS),  which takes into account the rim configuration adjusted for the disc size, can be used to minimise inter and intra-observer variation in disc evaluation
  • disc margin haemorrhage is an important prognostic sign but not necessarily diagnostic of glaucoma (more common in Normal Tension Glaucoma)
  • defects of the nerve fibre layer
  • if available, establish baseline imaging using OCT or fundus image to ascertain evidence of progressive change

Visual fields:

  • reproducible visual field test defect consistent with location of optic disc damage
  • relative or absolute arcuate scotoma, nasal step, paracentral loss, and in severe disease central island

Tonometry:

  • IOP is a modifiable risk factor and important measurement in the management of glaucoma (but not for diagnosis in isolation)
  • in a significant proportion of patients with glaucoma, IOP is in normal range (Normal Tension Glaucoma)
  • greater central corneal thickness produces artefactually high IOP measurements;
  • lesser central corneal thickness produces artefactually low IOP measurements
  • greater than normal diurnal variation in IOP (>4 mm Hg)
    • measure IOP at different times of day; usually highest in morning

Gonioscopy:

  • open angles with normal appearance
    • Shaffer Grading 3 or 4

Slit lamp assessment of limbal anterior chamber angle depth:

  • van Herick grading >25% (≥grade 3)

Open angle using anterior segment OCT (AS-OCT)

Differential diagnosis

Ocular hypertension (OHT)

  • defined as intraocular pressure above the normal range, without anterior segment abnormality, normal optic nerve and visual field
  • around 10% of untreated ocular hypertensives will develop glaucoma in 5 years
  • (See Clinical Management Guideline on Ocular Hypertension)

Tilted optic discs, physiological cupping, disc drusen, congenital optic nerve pit, anterior ischaemic optic neuropathy

Secondary glaucoma masquerading as COAG (e.g. steroid responder, pigment dispersion, pseudo-exfoliation)

Primary angle closure (PAC) / Primary angle closure glaucoma (PACG)

Neurological causes of optic neuropathy and visual field loss

Management by optometrist

Practitioners should work within their scope of practice, and where necessary seek further advice or refer the patient elsewhere

GRADE* Level of evidence and strength of recommendation always relates to the statement(s) immediately above

Non pharmacological

Guidance on glaucoma case finding is included in National Institute Health and Care Excellence (NICE) guideline (NG81, November 2017 [amended January 2022]): Glaucoma: diagnosis and management; Scottish Intercollegiate Guidelines Network guideline (SIGN 144, March 2015): ‘Glaucoma referral and safe discharge’ (see Evidence Base); and guidance produced by the College of Optometrists: ‘Examining patients at risk from glaucoma’. NICE guideline NG81 also provides detailed guidance on the diagnosis and management of COAG (including monitoring intervals)

Diagnosis: refer people with suspected optic nerve damage or repeated visual field defect (or both) to the Hospital Eye Service for consideration of a definitive diagnosis and formulation of a management plan (NICE recommendation).
(GRADE*: Level of evidence=low, Strength of recommendation=strong)

People with COAG should have monitoring and treatment from a trained healthcare professional who has all of the following: a specialist qualification in glaucoma; relevant experience; ability to detect a change in clinical status. Holding an independent or non-medical prescribing qualification alone (without a specialist qualification relevant to the case complexity of glaucoma being managed) is insufficient for managing glaucoma and related conditions (NICE recommendation).
(GRADE*: Level of evidence=low, Strength of recommendation=strong)

Offer people the opportunity to discuss their diagnosis, referral, prognosis, treatment and discharge, and provide them with relevant information in an accessible format at initial and subsequent visits. (NICE recommendation)
(GRADE*: Level of evidence=low, Strength of recommendation=strong)

There is evidence that primary selective laser trabeculoplasty (SLT) is a clinically effective and cost-effective alternative to ocular hypotensive drops. NICE updated its guidance (NG81) in January 2022 to recommend offering 360° SLT to people with newly diagnosed COAG (excluding cases associated with pigment dispersion syndrome).
(GRADE*: Level of evidence=moderate, Strength of recommendation=strong)

Pharmacological

Diagnosis: do not prescribe anti-glaucoma drugs prior to assessment by a consultant ophthalmologist (NICE recommendation). However, in collaboration with the local glaucoma service, treatment may be initiated by a prescribing optometrist with a specialist qualification in glaucoma on the basis of an initial diagnosis of COAG or for people who are awaiting SLT treatment
(GRADE*: Level of evidence=low, Strength of recommendation=strong)

Follow-up management: people with a diagnosis of POAG can be monitored (and treated) by optometrists with a specialist qualification in glaucoma (NICE recommendation)
(GRADE*: Level of evidence=low, Strength of recommendation=strong)
 

Management category

A3 (modified): Unless clinical circumstances indicate that urgent or emergency referral is indicated, patients should have referral filtering (e.g. repeat measures, referral refinement) before they are referred to the HES (NICE recommendation). The availability and type of referral filtering service may vary depending on local arrangements. In Scotland, referral criteria should follow SIGN guidelines.

Possible management in secondary care or local primary/community pathways where available

Additional guidance may be available

Confirmation of diagnosis of COAG
Determination of the individual clinical management plan 
Reduce IOP taking into account:

  • estimated target IOP for the individual patient
  • likely degree of compliance with medical therapy (the simpler, the better)
  • side effects, contra-indications and drug interactions
  • patient preferences and circumstances

Most people with COAG are treated with eye drops, but increasingly more people are offered SLT as first line therapy

  • prostaglandin analogues (latanoprost) are first choice
  • beta-blockers are second choice (relatively high incidence of unwanted effects)
  • other choices are carbonic anhydrase inhibitors and alpha agonists
  • systemic treatment for COAG is rarely needed. Long-term therapy with oral carbonic anhydrase inhibitors may be necessary in a few refractory cases but drug intolerance is common

Surgery (incisional or non-incisional) may be required. Primary trabeculectomy surgery is more effective in lowering IOP and preventing disease progression than primary medical treatment in patients with advanced disease. Increasingly, patients with mild/moderate glaucoma undergoing cataract surgery undergoing parallel microinvasive glaucoma surgery (MIGS).

Evidence base

*GRADE: Grading of Recommendations Assessment, Development and Evaluation (www.gradeworkinggroup.org)

Sources of evidence

Cheng KKW, Tatham AJ. Spotlight on the Disc-Damage Likelihood Scale (DDLS). Clin Ophthalmol. 2021;15:4059-4071.

Garway-Heath DF, Crabb DP, Bunce C, Lascaratos G, Amalfitano F, Anand N, Azuara-Blanco A, Bourne RR, Broadway DC, Cunliffe IA, Diamond JP, Fraser SG, Ho TA, Martin KR, McNaught AI, Negi A, Patel K, Russell RA, Shah A, Spry PG, Suzuki K, White ET, Wormald RP, Xing W, Zeyen TG. Latanoprost for open-angle glaucoma (UKGTS): a randomised, multicentre, placebo-controlled trial. Lancet. 2015; 4:385(9975),1295-304

Gazzard G, Konstantakopoulou E, Garway-Heath D, Garg A, Vickerstaff V, Hunter R, Ambler G, Bunce C, Wormald R, Nathwani N, Barton K, Rubin G, Buszewicz M; LiGHT Trial Study Group. Selective laser trabeculoplasty versus eye drops for first-line treatment of ocular hypertension and glaucoma (LiGHT): a multicentre randomised controlled trial. Lancet. 2019;393(10180):1505-1516

Gazzard G, Konstantakopoulou E, Garway-Heath D, Adeleke M, Vickerstaff V, Ambler G, Hunter R, Bunce C, Nathwani N, Barton K; LiGHT Trial Study Group. Laser in Glaucoma and Ocular Hypertension (LiGHT) Trial: Six-Year Results of Primary Selective Laser Trabeculoplasty versus Eye Drops for the Treatment of Glaucoma and Ocular Hypertension. Ophthalmology. 2023;130(2):139-151.

Ha A, Kim CY, Shim SR, Chang IB, Kim YK. Degree of myopia and glaucoma risk: a dose-response meta-analysis. Am J Ophthalmol. 2021;236:107-119

Hollands H, Johnson D, Hollands S, Simel DL, Jinapriya D, Sharma S. Do Findings on routine examination identify patients at risk for Primary Open-Angle Glaucoma? The Rational Clinical Examination Systematic Review. JAMA 2013;309(19):2035-42

King AJ, Hudson J, Azuara-Blanco A, Burr J, Kernohan A, Homer T, Shabaninejad H, Sparrow JM, Garway-Heath D, Barton K, Norrie J, Davidson T, Vale L, MacLennan G; TAGS Study Group∗. Evaluating Primary Treatment for People with Advanced Glaucoma: Five-Year Results of the Treatment of Advanced Glaucoma Study. Ophthalmology. 2024:S0161-6420(24)00016-2. doi: 10.1016/j.ophtha.2024.01.007. Online ahead of print.

NICE Guideline NG81 (2017 [amended 2022]). Glaucoma: diagnosis and management 

Rolim-de-Moura CR, Paranhos A Jr, Loutfi M, Burton D, Wormald R, Evans JR. Laser trabeculoplasty for open-angle glaucoma and ocular hypertension. Cochrane Database Syst Rev. 2022;8(8):CD003919. 

Scottish Intercollegiate Guidelines Network (SIGN). Glaucoma referral and safe discharge. Edinburgh: SIGN; 2015. (SIGN publication no. 144, March 2015). 

Vass C, Hirn C, Sycha T, Findl O, Sacu S, Bauer P, Schmetterer L. Medical interventions for primary open angle glaucoma and ocular hypertension. Cochrane Database of Systematic Reviews 2007;4:CD003167

Zhou M, Wang W, Huang W, Zhang X. Diabetes mellitus as a risk factor for open-angle glaucoma: a systematic review and meta-analysis. PLoS One. 2014 Aug 19;9(8):e102972)

Summary

What is Chronic Open Angle Glaucoma?

Chronic Open Angle Glaucoma (COAG) affects approximately 1-2% of the white population of the UK over 40 years of age, increasing to 4-5% of those over 80 years. It is more likely to affect people with a family history of the same condition, and people of West African ancestry, including African-Caribbean. The condition is not painful and patients may be unaware that they have it until they have started to lose vision.

The optometrist examining a patient for COAG, will look for the characteristic appearance of ‘cupping’ of the optic disc (the head of the optic nerve at the back of the eye). The optic nerve transfers visual information from the eye to the brain, and can be examined with various special instruments. On testing the patient’s fields of vision, defects may be found that are typical of glaucoma. The pressure of the fluid inside the eye (known as the intraocular pressure) must be measured as it is usually raised in glaucoma. In a small proportion of patients, however, the pressure is within the normal range.

The eyeball is a sphere kept inflated by fresh clear fluid formed within the eye. This fluid drains away through a fine ring-shaped sieve of tissue, known as the drainage angle (or simply angle), situated within the eye at the edge of the cornea (the clear window of the eye) and from there into the bloodstream. This sieve is not directly visible but it can be seen through a special contact lens containing a mirror. In COAG the fluid is unable to escape normally because the meshwork has become blocked. The blockage causes the pressure inside the eye to rise, and in time this can damage the optic nerve, causing loss of visual field and even blindness if the condition is not treated. 

How is Chronic Open Angle Glaucoma managed?

Treatment is usually with eye drops, or with a laser procedure called selective laser trabeculoplasty (SLT) which lower the intraocular pressure. If these treatments are inadequate a separate operation may be needed.

The optometrist who discovers COAG will usually refer the patient routinely to the hospital eye service. 

Sometimes COAG develops out of another condition called Ocular Hypertension, for which a separate Clinical Management Guideline has been written.

Last updated

Glaucoma (chronic open angle) (COAG)
Version 18
Date of search 13.05.24
Date of revision 20.06.24
Date of publication 22.07.24
Date for review 12.05.26
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