«GUIDELINES FOR THE MANAGEMENT OF OPEN ANGLE GLAUCOMA AND OCULAR HYPERTENSION 2004 THE SCIENTIFIC DEPARTMENT THE ROYAL COLLEGE OF OPHTHALMOLOGISTS 17 ...»
THE ROYAL COLLEGE OF OPHTHALMOLOGISTS
GUIDELINES FOR THE MANAGEMENT OF OPEN ANGLE GLAUCOMA
AND OCULAR HYPERTENSION
THE SCIENTIFIC DEPARTMENT
THE ROYAL COLLEGE OF OPHTHALMOLOGISTS
17 CORNWALL TERRACE
LONDON NW1 4QW
TELEPHONE: 020 7935 0702
FACSIMILE: 020 7487 4674 WWW.RCOPHTH.AC.UK
CONTENTSI Executive Summary 4 II Introduction 5 III Ocular hypertension 6
2. Risk factors for the development of ocular hypertension
4. Risk factors for conversion to glaucoma
5. Prophylactic therapy
6. Some guidelines on treatment IV. Primary open angle glaucoma (chronic simple glaucoma) 11
2. Prevalence and natural history
3. Risk factors for the development of POAG
4. Risk factors for blindness in POAG
6. Glaucoma without field loss
7. Concepts in glaucoma management
8. Monitoring the patient with POAG
9. Management of the patient who demonstrates progression
10. Normal tension glaucoma 2 V. The Treatment of primary open angle glaucoma 18
2. Laser surgery
3. Surgical VI Social and practical aspects of glaucoma 22
1. Information concerning drop utilisation
2. Registration as partially sighted and legally blind
3. Glaucoma and driving
4. Informing relatives of their risk of glaucoma
5. Help agencies and glaucoma
6. Utilising written information VII. References 24 VIII. Working Party and acknowledgements 29 3
I. EXECUTIVE SUMMARYThe management of patients with ocular hypertension and primary open angle glaucoma accounts for a significant proportion of the workload of most ophthalmologists. This document should not be considered to be a protocol for management, but rather consensus guidelines that outline the definitions, epidemiology, and concepts in management of these chronic conditions. The comments expressed in these guidelines incorporate the results from recent randomised controlled trials published up to Dec 2002 as well as consensus views derived from experience where evidence from prospective trials was not available.
Low-tension (or normal tension) glaucoma is considered, for the purposes of the document, to be a subgroup of primary open angle glaucoma. Where intraocular pressure is mentioned, measurement is considered to have been with a calibrated Goldmann tonometer.
Shared care is not discussed, the reader being referred to the current guidelines published by The Royal College of Ophthalmologists on this topic.
These guidelines should be updated before June 2008 at the latest.
Glaucoma causes significant visual disability in the UK, accounting for 15% of registrable blindness. This figure probably underestimates the morbidity since many patients who are eligible for registration do not appear in the statistics.
The management of patients with primary open angle glaucoma (POAG) and ocular hypertension (OHT) constitutes a major part of the workload of the general ophthalmologist.
Approximately 25% of follow up attendances and 15% of new referrals either are glaucoma suspects or have glaucoma. It is estimated that there are an equal number of undiagnosed glaucoma patients in the community as there are attending eye clinics. As the population ages, case detection improves and evidence for early treatment for OHT accumulates, the number of referrals to ophthalmologists for suspect glaucoma and OHT is likely to increase.
1. Definition Ocular hypertension (OHT) is a term reserved for eyes in which the intraocular pressure (IOP) lies above the normal population range, the optic nerve and visual field show no signs of glaucomatous damage, and there is no ocular co-morbidity. Excluded from this definition are eyes with raised IOP from demonstrable causes such as pseudoexfoliation and pigment dispersion syndrome.
Most population studies on the over 40-year age group indicate that IOPs measured with Goldmann tonometry are distributed in a manner similar to a normal distribution (mean approximately 16 mmHg). Persons with IOPs greater than two standard deviations above the mean can be labelled Ocular Hypertensive. This gives an upper limit for “normal” IOPs in Caucasians of 21 mmHg. It is of note however that this figure is statistically derived and does not imply that disease is present if measured IOP levels exceed this value.
Individuals with OHT account for 5 - 6% rather than the 2.5% that would be expected from a true normal distribution. It is becoming recognised that while these figures are true for Caucasian populations they may not hold true for other ethnic groups where the mean IOP may be lower (e.g. the Japanese are reported to have a lower mean IOP).
Epidemiological studies have identified those individuals in a population most at risk :Increasing age
2. Individuals of black African or Caribbean origin.
3. Female gender
4. Systemic hypertension
5. Current use of oral and/or inhaled corticosteroids
6. Diabetes (especially those on insulin)
7. Family history of glaucoma
3. Management Since elevated IOP is the major risk factor for the development of glaucomatous visual loss, finding a "raised" IOP indicates the need for further investigation and management decisions. Most ocular hypertensives are detected in optometric practice and several scenarios are possible at ophthalmological examination after referral:An "unconfirmed" raised IOP at screening - the ophthalmologist finds a "normal" IOP and no evidence of any other abnormality (remember the various causes of artifactually raised IOP measurements especially “Valsalva”).
2. Intermittent OHT - raised IOP is confirmed initially but reverts to normal on repeated testing over time and no evidence of any other related abnormality is detected.
3. "Persistent" OHT where raised IOP is a constant feature.
Assuming an otherwise normal ocular examination, patients in categories 1 and 2 can be discharged and advised to seek periodic (e.g. one to two yearly) optometric re-examination.
Patients in category 3 require the ophthalmologist to make a decision on the appropriate follow up and possible prophylactic treatment.
74. Risk factors for conversion to glaucoma
Estimates vary as to the conversion rate from OHT to POAG, depending on subject selection and diagnostic criteria. It is likely that approximately 10% of individuals with persistent OHT will convert to POAG over a ten-year period. Risk factors for the conversion of OHT to POAG can be divided into ocular and systemic. The most important are listed below
A. Ocular risk factors
Height of the IOP - the greater the IOP the greater the risk
• Large vertical cup/disc ratio (indicating reduced neuroretinal rim area/volume)
• Cup/disc (C/D) ratio asymmetry 0.2
• Previous history of disc haemorrhage
• Retinal nerve fibre layer defect in the absence of morphometric optic nerve head changes
• Thinner than average central corneal thickness (note excimer laser procedures on the cornea can result in artifactually lowered IOPs on measurement) B. Systemic risk factors
• Increasing age
• Family history
• Individuals of black African or Caribbean origin
A decision to treat an eye with ocular hypertension should be made when the risk factor(s) present in the patient are considered to outweigh the disadvantages of treatment.
Indications include the presence of signs suggestive of early glaucoma or central retinal vein occlusion in the fellow eye.
If no treatment is decided upon, two options are available to the ophthalmologist.
• Discharge to the GP with appropriate advice for follow-up in the community.
• Periodic review in the Hospital Eye service or managed shared care scheme.
The former is acceptable in low risk cases. If the latter is chosen, re-examination to assess IOP, visual field and optic disc should occur at intervals considered appropriate for the patient. Observation either in the HES or the community should employ methods sufficiently accurate and dependable to give the patient the best chance of identifying conversion to glaucoma at the earliest possible opportunity.
6. Some guidelines on treatment
When treating OHT, the aim is to lower the IOP to a level considered safe for the individual patient, and this should be at least a 20% reduction. It should be emphasised that treatment should only be advised following a careful evaluation of the full implications of treating the individual concerned, including a realistic assessment of the inconvenience and potential side effects of such treatment.
A. Treating on IOP without additional risk factors.
A constant IOP over 35 mmHg merits treatment as at these levels mechanical damage occurs to the optic nerve head. Many specialists would treat when the IOP is consistently 28-30 mmHg or above in the absence of other risk factors. The decision to initiate treatment at a lower level of IOP should be based on perceived risk by the ophthalmologist and the patient (see over).
9B. Treating on raised IOP plus other risk factors.
The recently published Ocular Hypertension Treatment Study (OHTS) provides figures for risk, adjusted according to the height of the IOP, the central corneal thickness and the vertical C/D ratio. When these factors combine to give an appreciable 5-year risk of developing a significant optic disc change or a visual field defect, the ophthalmologist needs to identify this to the patient and outline the benefits and risks of treatment. This is particularly important if a decision is made to withhold treatment at this stage. The decision to treat should take into account the patient’s life expectancy and the probability of functional visual loss occurring within the patient’s lifetime.
Eyes that already possess evidence of early glaucomatous damage such as acquired neuroretinal rim changes consistent with glaucoma, nerve fibre layer defects or abnormalities on morphometric, psychophysical or electrodiagnostic tests probably have POAG and should be treated as such (see Concepts in glaucoma management page 13).
Primary open angle glaucoma (POAG) is a chronic progressive condition with characteristic changes at the optic disc (glaucomatous excavation), where it is usually possible to identify reduced visual function related to the disc changes. In most patients, the IOP is above the normal range (i.e. over 21 mmHg) at some time of the day, usually being highest in the morning. In addition, there is a gonioscopically open angle indistinguishable from normal and, in those eyes with elevated IOP, a reduced facility of outflow.
2. Prevalence and natural history
In a white population, POAG occurs in approximately 1-2% of the population over 40, increasing with age to 4% or more of the over 80-year olds. Exact prevalence rates vary depending on the criteria used for diagnosis. Left untreated, the natural history of the disease is to progress, leading to irreversible blindness. The two published population based incidence studies (from Baltimore and Melbourne) both found that about 40% of the converters had normal baseline IOPs. The Baltimore incidence study found a progressive increase in risk with increasing IOP at baseline.
3. Risk factors for the development of POAG In addition to the risk factors already outlined for the conversion of OH to POAG, the following additional risk factors have been cited as playing a role in the development of POAG.
• Positive family history in a first degree relative
• High myopia
• Diabetes (equivocal evidence)
• Advanced disease at presentation
• Sub-optimal intraocular pressure control
• Individuals of black African or Caribbean origin
• Low socio-economic group (because of late presentation) It is obvious that in an individual patient, the attending ophthalmologist can only influence the second of these listed risk factors. It should also be noted that some patients continue to lose vision from glaucoma despite an IOP maintained at an acceptable level.
5. Diagnosis POAG can occur in eyes with normal or raised IOP. The concept that POAG only occurs with pressures over 21 mmHg is incorrect. Increasing emphasis has therefore been placed upon:The morphological changes occurring at the optic nerve head and retinal nerve fibre layer.
2. The alterations in psychophysical tests that glaucomatous damage causes.
6. Glaucoma without field loss detected on standard automated “white on white” perimetry (SAP) The discovery that a significant number of the optic nerve fibres can be damaged before any change is detectable in visual function by SAP has lead to the concept of "glaucoma without field loss" or “pre-perimetric glaucoma”. However other psychophysical tests such as frequency doubled perimetry (FDP) and blue on yellow perimetry (SWAP) have consistently shown that defects in visual function are present before any defect can be detected by SAP.
In this condition (usually with coexistent raised IOP) there is deemed to be unequivocal evidence of glaucomatous damage to the optic nerve head +/- the nerve fibre layer. Clearly, for some patients, there is a grey area between OHT and "glaucoma without field loss".
127. Concepts in glaucoma management
The overall aim of glaucoma management is to prevent significant visual impairment within the patient’s lifetime. This will be achieved by a process of monitoring visual function with medical and/or surgical intervention when appropriate. Treatment may, therefore, not always be necessary to achieve this objective.