1Introduction

Publication Details

1.1. What is a guideline?

Our clinical guidelines are recommendations for the care of individuals in specific clinical conditions or circumstances within the NHS – from prevention and self-care through primary and secondary care to more specialised services. We base our clinical guidelines on the best available research evidence, with the aim of improving the quality of health care. We use predetermined and systematic methods to identify and evaluate the evidence relating to specific clinical questions.

Clinical guidelines can:

  • provide recommendations for the treatment and care of people by health professionals
  • be used to develop standards to assess the clinical practice of individual health professionals
  • be used in the education and training of health professionals
  • help patients to make informed decisions
  • improve communication between patient and health professional

While guidelines assist the practice of healthcare professionals, they do not replace their knowledge and skills.

We produce our guidelines using the following steps:

  • Guideline topic is referred to NICE from the Department of Health
  • Stakeholders register an interest in the guideline and are consulted throughout the development process.
  • The scope is prepared by the National Collaborating Centre for Acute Care (NCC-AC)
  • The National Collaborating Centre for Acute Care establish a guideline development group
  • A draft guideline is produced after the group assesses the available evidence and makes recommendations
  • There is a consultation on the draft guideline.
  • The final guideline is produced.

The National Collaborating Centre for Acute Care and NICE produce a number of versions of this guideline:

  • the full guideline contains all the recommendations, plus details of the methods used and the underpinning evidence
  • the NICE guideline presents the recommendations from the full version in a format suited to implementation by health professionals and NHS bodies
  • the quick reference guide presents recommendations in a suitable format for health professionals
  • information for the public (‘understanding NICE guidance’) is written using suitable language for people without specialist medical knowledge.

This version is the full version. The other versions can be downloaded from NICE www.NICE.org.uk.

1.2. The need for this guideline

Chronic open-angle glaucoma tends to be asymptomatic and therefore many people will not notice any symptoms until severe visual damage has occurred. Once diagnosed, affected individuals require lifelong monitoring for disease control and detection of prossible progression of visual damage. It is estimated that in the UK about 2% of people older than 40 years have chronic open angle glaucoma, and this rises to almost 10% in people older than 75 years. There are around 480,000 people affected by chronic open angle glaucoma in England, who receive over a million glaucoma related outpatient visits in the hospital eye service annually. With changes in population demographics the number of people affected by glaucoma is expected to rise. Approximately 10% of UK blindness registrations are ascribed to glaucoma, and since with appropriate treatment blindness is largely avoidable, this figure suggests that there may be room for improvements both in case ascertainment and ongoing care following diagnosis.

A plethora of topical medications and combinations of medications are available for treatment of COAG. In addition there exist a number of laser and surgical procedures which may be used to reduce IOP and arrest or slow progression of vision loss. There are wide variations across the NHS in terms of management of COAG, a reflection of the uncertainties and sometimes conflicting reports in the scattered literature. Recent evidence indicates that treating elevated IOP prior to the onset of glaucoma reduces by half the risk of conversion from OHT to COAG. Whether such preventative treatment is cost effective in terms of long term avoidance of blindness has been unclear.

Service pressures and centrally imposed imperatives to bring down waiting times in the NHS by prioritisation of new referrals has in many areas displaced capacity away from chronic disease monitoring with consequent cancellations and long delays in follow up appointments. Such distortions of clinical practice, where a new referral for someone who may or may not have a significant eye problem gains priority over a patient with a diagnosed and potentially blinding eye disease has resulted in service failures for individuals and cannot be accepted. Guidance on chronic disease monitoring, including monitoring intervals and service models, is therefore timely. Lord Darzi’s quality initiative provides an opportune backdrop for a rebalancing of service priorities towards overall clinical need, inclusive of long term conditions such as chronic open angle glaucoma.

1.3. The National Collaborating Centre for Acute Care

This guideline was commissioned by NICE and developed by the National Collaborating Centre for Acute Care (NCC-AC). The centre is funded by NICE and comprises a partnership between a variety of academic, professional and patient-based organisations. As a multidisciplinary centre we draw upon the expertise of the healthcare professions and academics and ensure the involvement of patients in our work.

On the 1st April 2009 the NCC-AC merged with three other NCCs (Primary Care, Chronic Conditions and Nursing and Supportive Care) to form the National Clinical Guidelines Centre for Acute and Chronic Conditions (NCGC-ACC).

1.4. Remit

The following remit was received by the NCC-AC from the Department of Health in January 2006 as part of NICE’s 12th wave programme of work.

The Department of Health asked the Institute:

“To prepare a clinical guideline on the diagnosis and management of chronic open angle glaucoma and ocular hypertension (raised intraocular pressure). The guideline should include recommendations on the most appropriate service models where evidence of effectiveness is available.”

1.5. What the guideline covers

This guideline covers adults (18 and older) with a diagnosis of chronic open angle glaucoma or ocular hypertension and those with chronic open angle glaucoma or ocular hypertension associated with pseudoexfoliation or pigment dispersion. In addition, the guideline will cover populations who have a higher prevalence of glaucoma and may have worse clinical outcomes including people with a family history of glaucoma, younger people (<50 years) and people who are of black African or black Caribbean descent. Options for pharmacological, surgical, laser and complimentary or alternative treatments are considered in terms of clinical effectiveness and cost effectiveness. Further details of the scope of the guideline can be found in Appendix A.

1.6. What the guideline does not cover

This guideline does not cover patients under the age of 18 years. In addition, the guideline does not cover patients with secondary glaucoma (for example neovascular or uveitic) except for those described above, those with, or at risk of, primary or secondary angle closure glaucoma and adults with primary congenital, infantile or childhood glaucoma.

1.7. Who developed this guideline?

A multidisciplinary Guideline Development Group (GDG) comprising professional group members and consumer representatives of the main stakeholders developed this guideline (see section on Guideline Development Group Membership and acknowledgements).

The National Institute for Health and Clinical Excellence funds the National Collaborating Centre for Acute Care (NCC-AC) and thus supported the development of this guideline. The GDG was convened by the NCC-AC and chaired by Mr. John Sparrow in accordance with guidance from the National Institute for Health and Clinical Excellence (NICE).

The group met every 6–8 weeks during the development of the guideline. At the start of the guideline development process all GDG members declared interests including consultancies, fee-paid work, share-holdings, fellowships and support from the healthcare industry. At all subsequent GDG meetings, members declared arising conflicts of interest, which were also recorded (Appendix B).

Members are either required to withdraw completely or for part of the discussion if their declared interest makes it appropriate, however this was not deemed necessary for any group members on this guideline.

Staff from the NCC-AC provided methodological support and guidance for the development process. They undertook systematic searches, retrieval and appraisal of the evidence and drafted the guideline. The glossary to the guideline contains definitions of terms used by staff and the GDG.

1.8. Assumptions made

1.8.1. Ocular Hypertension (OHT)

The GDG agreed the following assumptions regarding the definition of ocular hypertension:

  • open drainage angles on gonioscopy
  • an untreated IOP above 21mmHg, confirmed on a separate occasion
  • absence of typical optic disc damage (e.g. glaucomatous cupping and loss of neuroretinal rim)
  • absence of detectable nerve fibre layer defect
  • absence of visual field defect
  • included variants:
    • OHT with pigment dispersion
    • OHT with pseudo-exfoliation
  • absence of other secondary cause for IOP elevation (e.g. trauma, uveitis)

1.8.2. Chronic open-angle glaucoma suspect (COAG Suspect)

The GDG agreed the following assumptions regarding the definition of suspected COAG:

  • open drainage angles on gonioscopy
  • 1 or more of:
    • possible optic disc damage with suspicion of glaucomatous cupping
    • possible optic disc damage with suspicion of loss of neuroretinal rim
    • possible nerve fibre damage with suspicion of nerve fibre layer defect
    • normal or equivocal visual field
  • included variants
    • COAG Suspect with pigment dispersion
    • COAG Suspect with pseudo-exfoliation
    • COAG Suspect with repeatedly elevated untreated IOP (above 21mmHg) identified as Primary Open Angle (POAG) Suspect
    • COAG Suspect with repeatedly normal untreated IOP (21mmHg or less) identified as Normal Tension Glaucoma (NTG) Suspect
  • absence of other secondary cause for IOP elevation if present (e.g. trauma, uveitis)

1.8.3. Chronic open-angle glaucoma (COAG)

The GDG agreed that the following assumptions would normally apply regarding the definition of COAG:

  • open drainage angles on gonioscopy
  • visual field damage compatible with nerve fibre loss
  • 1 or more of
    • optic disc damage with glaucomatous cupping
    • optic disc damage with loss of neuroretinal rim
    • nerve fibre damage with nerve fibre layer defect
  • included variants
    • COAG with repeatedly elevated untreated or treated IOP (above 21mmHg) identified as Primary Open Angle (POAG)
    • COAG with repeatedly normal untreated IOP (21mmHg or less) identified as Normal Tension Glaucoma (NTG)
    • COAG with pigment dispersion
    • COAG with pseudo-exfoliation
  • absence of other secondary cause for IOP elevation (e.g. trauma, uveitis)

1.8.4. Glaucomatous changes to the optic nerve

Glaucomatous changes to the optic nerve may include:

  • Features strongly suggestive of optic nerve damage:
    • Localised or generalised thinning of the neuro-retinal rim
    • Notches in the neuro-retinal rim
    • Optic nerve head haemorrhages without apparent secondary cause (e.g. diabetes)
    • Evidence of nerve fibre layer tissue loss (not always visible)
    • Vertical cup to disc ratio >0.85 (less in the presence of a small sized optic disc)
  • Features suggestive of possible optic nerve damage:
    • Cup-to-disc ratio Asymmetry >0.2
    • Cup-to-disc > 0.6
    • Nasal cupping
    • Peri-papillary atrophy
    • Neuro-retinal rim thinning with possible disturbance of the ‘Inferior- Superior – Nasal – Temporal’ pattern (ISNT rule)
    • Deep cup with prominent lamina cribrosa (soft sign)
    • Bayoneting of the optic nerve head vessels (soft sign)

1.8.5. Glaucomatous changes of the visual field

Glaucomatous changes of the visual field which reflect nerve fibre bundle loss include one or more of the following in the absence of other ocular or neurological disease affecting the visual field:

  • Unequivocal:
    • Arcuate Scotomas in the 30 degree central field
    • Nasal Steps
    • Altitudinal Scotomas
    • Focal Defects e.g. paracentral scotomas
    • Absolute defects
  • Suspicious:
    • Generalised defect
    • Relative defect
    • Enlarged blind spot

1.8.6. Stages of glaucomatous visual field loss

Glaucomatous visual field loss is defined by Hodapp Classification63 as below:

  • Early:
    • Mean Defect > -6dB
    • 5% Probability level defect for < 18 of tested points (tested field locations)
    • 1% Probability level defect for < 10 of tested points
  • Moderate:
    • Mean Defect -6dB > -12dB
    • 5% Probability level defect for < 37 of tested points
    • 1% Probability level defect for < 20 of tested points
    • Sensitivity <15dB in central 5 degrees on only one hemifield
  • Advanced:
    • Mean Defect -12dB > -20
    • 5% Probability level defect for > 37 of tested points
    • 1% Probability level defect for > 20 of tested points
    • Sensitivity <15dB in central degrees on both hemifield

1.8.7. Target IOP

The setting of a target IOP is a clinical decision and it may be necessary to change the target through the course of the disease. General principles will include the notion of a reduction of 25%–30% from the untreated pressure for cases of COAG and an IOP below 21mmHg for cases of ocular hypertension. Consideration should be given to the perceived threat to sighted lifetime, status of fellow eye, adherence to treatment, the likelihood of surgical success and patient preferences regarding treatment options.

1.8.8. Progression

Progression may be considered to have occurred when there is reliable evidence that visual field damage and / or glaucomatous optic neuropathy has worsened significantly. Since COAG is defined as a ‘progressive optic neuropathy’ a key concept in its management is the rate of progression. In spite of treatment most glaucoma will continue to progress. The aim of lowering IOP is to slow the rate of progression and the main treatment challenge is to avoid loss of sight and disability within a patient’s expected lifetime.

1.8.9. Pseudoexfoliation and pigment dispersion

Patients with the variants pseudoexfoliation and pigment dispersion would be expected to follow a slightly different natural history and in accordance with such variations informed clinical judgment should be used to maintain optimal care.

1.8.10. Severe Visual Impairment

There is no legal definition of sight impairment. The guidelines are that a person can be certified as sight impaired if they are ‘substantially and permanently handicapped by defective vision caused by congenital defect or illness or injury’. The National Assistance Act 1948 states that a person can be certified as severely sight impaired if they are “so blind as to be as to be unable to perform any work for which eye sight is essential” (National Assistance Act Section 64(1)).128

For the purposes of the economic analysis the definition of severe visual impairment was considered by the GDG to be:

  • Mean Defect <-20 dB

It was further assumed that both eyes were similar.

1.8.11. Risk factors for patients with COAG

Evidence of benefit from differentially treating patients with particular risk factors was not found. The rate of progression to vision loss may however vary between certain patient groups using standard treatment regimes and those perceived clinically to be at higher risk may need a lower target IOP.