Glaucoma (primary open angle) (POAG)

The CMGs are guidelines on the diagnosis and management of a range of common and rare, but important, eye conditions that present with varying frequency in primary and first contact care.

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Aetiology

Primary Open Angle Glaucoma 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 1-2% of the white population of the UK aged over 40 years, increasing to 4-5% in the over-80s
Second most common cause of irreversible blindness in the UK (approx. 10% of blind registrations)
Incidence: M = F

Predisposing factors

Ocular hypertension
Increasing age
Positive family history in a first degree relative
People of West African descent including West Indians and African Americans; onset at younger age
Thinner central cornea
Myopia > 3D (odds ratio = 2.46)
Diabetes (odds ratio = 1.35)
Systemic hypertension

Symptoms

Usually asymptomatic until there is significant loss of visual field

Signs

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 or R:L asymmetry ≥ 0.2 suspicious of glaucoma
  • 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 visible in younger patients
  • if available, establish baseline using stereo-photography or with computer-based image analysis e.g. confocal scanning laser ophthalmoscope (CSLO) or ocular coherence tomography (OCT)

Visual fields:

  • reproducible visual field test defect consistent with optic disc appearance
  • relative or absolute arcuate scotoma, nasal step, paracentral loss

Applanation tonometry:

  • IOP >21mmHg
    • greater central corneal thickness produces artefactually high IOP measurements
    • lesser central corneal thickness produces artefactually low IOP measurements

NB: in a significant proportion of patients with glaucoma, IOP is in normal range (Normal Tension Glaucoma)

  • 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

Assessment of anterior chamber angle depth at slit lamp:

  • van Herick Grading (limbal anterior chamber depth >25% of corneal thickness [Grade 3 or 4])

Differential diagnosis

Ocular hypertension (OHT)

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

Tilted optic discs, physiological cupping, disc drusen, anterior ischaemic optic neuropathy
Secondary glaucoma masquerading as POAG (e.g. steroid responder, pigment dispersion, pseudo-exfoliation)
Primary angle closure (PAC) / Primary angle closure glaucoma (PACG)

Management by optometrist

Practitioners should recognise their limitations 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): 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 POAG (including monitoring intervals)

Diagnosis: refer people with suspected optic nerve damage or repeated visual field defect (or both) to a consultant ophthalmologist 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 POAG 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)
 

Pharmacological

Diagnosis: do not prescribe anti-glaucoma drugs prior to assessment by a consultant ophthalmologist (NICE recommendation)
(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): In England, unless clinical circumstances indicate that urgent or emergency referral is indicated, patients should have referral filtering (e.g. repeat masures, referral refinement) before they are referred to the HES. In Scotland, referral criteria should follow SIGN guidelines

Possible management by ophthalmologist

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

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

Most POAG is treated with eye drops

  • prostaglandin analogues are first choice
  • beta-blockers are second choice (relatively high incidence of unwanted effects)
  • other choices are carbonic anhydrase inhibitors and alpha agonists
  • Selective Laser Trabeculoplasty (SLT) is increasingly used as a first line treatment
  • systemic treatment for POAG 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

Evidence base

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

Sources of evidence

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

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

Marcus MW, de Vries MM, Junoy Montolio FG, Jansonius NM. Myopia as a risk factor for open-angle glaucoma: a systematic review and metaanalysis. Ophthalmology. 2011;118(10):1989-1994

NICE Guideline NG81 (2017). Glaucoma: diagnosis and management https://www.nice.org.uk/guidance/ng81

Scottish Intercollegiate Guidelines Network (SIGN). Glaucoma referral and safe discharge. Edinburgh: SIGN; 2015. (SIGN publication no. 144, March 2015). http://www.sign.ac.uk

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)

Lay summary

Primary Open Angle Glaucoma (POAG) 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 West Indians and African Americans. 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 POAG, 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, or IOP) 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 POAG 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. Treatment is usually with eye drops, which slow the production of fluid or increase its drainage, but if these are inadequate an operation may be needed.

The optometrist who discovers POAG will usually refer the patient routinely to the ophthalmologist. 

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

Glaucoma (primary open angle) (POAG)
Version 15
Date of search 17.12.17
Date of revision 19.04.18
Date of publication 09.05.18
Date for review 16.12.19
© College of Optometrists 

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