Glaucoma
Glaucoma - Summary
Glaucoma is a group of eye diseases in which progressive damage to the optic nerve leads to impaired vision and, in a small proportion of people, blindness.
It is characterized by:
Visual field defects — arcuate scotomas, nasal steps, and altitudinal loss.
Changes to the head of the optic nerve — pathological cupping and, as a late sign, pallor of the optic disc.
Nerve fibre layer defects.
Suspected glaucoma is defined as changes in the optic nerve head (optic disc) or visual field that inconclusively suggest glaucomatous damage (regardless of the intraocular pressure).
Ocular hypertension is a condition defined by consistently or recurrently elevated intraocular pressure (greater than 21 mmHg) and no signs of glaucoma.
Glaucoma is described in four main ways, according to:
Age of onset: congenital, infantile, juvenile, or adult.
Rate of onset: acute or chronic.
Cause: primary (no known cause), or secondary, with a known cause such as a disease, drug, or developmental condition that increases intraocular pressure and damages the optic nerve.
Mechanism: angle closure glaucoma or open angle glaucoma.
Acute angle closure glaucoma should be suspected in someone who presents with an acute painful red eye and:
Is female, Asian, long-sighted, or of older age.
Has a history of previous episodes of blurred vision, headaches, or eye pain associated with nausea and seeing halos around lights; these symptoms typically occur in the evening and are relieved by sleeping.
Has a history of a precipitating factor such as use of an adrenergic drug (for example phenylephrine) or an antimuscarinic drug (for example a tricyclic antidepressant).
Has the following symptoms and signs: headache, nausea, and vomiting caused by the painful eye; lights are seen surrounded by halos — caused by a hazy oedematous cornea; semi-dilated and fixed pupil; tender, hard eye; impaired visual acuity; optic disc is oedematous and hyperaemic, with engorged blood vessels.
If acute angle closure glaucoma is suspected, the person should be referred immediately for specialist ophthalmology assessment and treatment.
If immediate admission is not possible, it is recommended that emergency treatment is started in primary care.
If the person lies flat with their face up and head not supported by pillows, this may relieve some of the pressure on the angle.
If available, the following drugs should be given:
Pilocarpine one drop of 2% in blue eyes or 4% in brown eyes.
Acetazolamide 500 mg orally to reduce production of aqueous humour, provided that there are no contraindications.
Analgesia.
Anti-emetic, if required.
If a primary healthcare professional suspects chronic open angle glaucoma, they should refer the person non-urgently to an optometrist or ophthalmologist.
Treatment of confirmed chronic open angle glaucoma, and treatment of ocular hypertension when indicated, are initiated and monitored by specialists.
Primary care healthcare professionals may be involved in continuing shared care.
Have I got the right topic?
This CKS topic is based on the guideline Glaucoma: diagnosis and management of chronic open angle glaucoma and ocular hypertension developed by the National institute for Health and Clinical Excellence (NICE) [National Collaborating Centre for Acute Care, 2009a] and takes account of guidelines developed by the College of Optometrists and by the Royal College of Ophthalmologists [The College of Optometrists, 2009a; The College of Optometrists, 2009c; The College of Optometrists, 2009d; The College of Optometrists and The Royal College of Ophthalmologists, 2009].
This CKS topic covers the recognition and management in primary care of chronic open angle glaucoma and ocular hypertension. The primary care management of angle closure glaucoma (which is outside the scope of the NICE guideline) is only briefly covered.
This CKS topic does not cover secondary glaucoma, or congenital, infantile, or juvenile glaucoma.
There is a separate CKS topic on Red eye.
The target audience for this CKS topic is healthcare professionals working within the NHS in the UK, and providing first contact or primary healthcare.
How up-to-date is this topic?
How up-to-date is this topic?
Changes
April 2011 — minor update. NICE quality standards on the management of glaucoma added to the Goals and outcome measures section. Issued in June 2011.
September 2010 — minor correction to ensure the term 'chronic open angle glaucoma' is used consistently.
May to September 2010 — this is a new CKS topic. The evidence-base has been reviewed in detail, and recommendations are clearly justified and transparently linked to the supporting evidence.
Update
New evidence
Evidence-based guidelines
Guidelines published since the last revision of this topic:
College of Optometrists and Royal College of Ophthalmologists (2013) Commissioning better eye care. Clinical commissioning guidance from the College of Optometrists and the Royal College of Ophthalmologists. Glaucoma. College of Optometrists and Royal College of Ophthalmologists. www.college-optometrists.org [Free Full-text]
HTAs (Health Technology Assessments)
No new HTAs since 1 May 2010.
Economic appraisals
No new economic appraisals relevant to England since 1 May 2010.
Systematic reviews and meta-analyses
Systematic reviews published since the last revision of this topic:
Boland, M.V., Ervin, A., Friedman, D.S., et al. (2013) Comparative effectiveness of treatments for open-angle glaucoma: a systematic review for the U.S. Preventive Services Task Force. Annals of Internal Medicine 158(4), 271-279. [Free Full-text]
Li, M., Wang, M., Guo, W., et al. (2011) The effect of caffeine on intraocular pressure: a systematic review and meta-analysis. Graefe's Archives for Clinical & Experimental Ophthalmology 249(3), 435-442. [Abstract]
Marcus, M.W., de Vries, M.M., Montolio, F.G. and Jansonius, N.M. (2011) Myopia as a risk factor for open-angle glaucoma: a systematic review and meta-analysis. Opthalmology 118(10), 1989-1994.e2. [Abstract]
Webers, C.A., Beckers, H.J., Zeegers, M.P., et al. (2010) The intraocular pressure-lowering effect of prostaglandin analogs combined with topical beta-blocker therapy: a systematic review and meta-analysis. Ophthalmology 117(11), 2067-2074. [Abstract]
Primary evidence
No new randomized controlled trials published in the major journals since 1 May 2010.
New policies
No new national policies or guidelines since 1 May 2010.
New safety alerts
No new safety alerts since 1 May 2010.
Changes in product availability
No changes in product availability since 1 May 2010.
Goals and outcome measures
Goals
To support primary healthcare professionals:
To advise people at high risk of chronic open angle glaucoma to have their eyes examined by an optometrist
To provide shared care for people who are being treated for chronic open angle glaucoma or ocular hypertension in secondary care
To recognize and refer people with acute angle closure glaucoma
Audit criteria
The National Institute for Health and Clinical Excellence (NICE) have published audit criteria for use by NHS eye services.
NICE quality standards
NICE quality standards
People are referred to a consultant ophthalmologist for further assessment and definitive diagnosis if the optometrist or other healthcare professional suspects COAG. There are local agreements in place for referral refinement.
People with elevated IOP alone are referred to an appropriately qualified healthcare professional for further assessment on the basis of perceived risk of progression to COAG. There are agreements in place for repeat measures.
People referred for definitive diagnosis in the context of possible COAG or with OHT receive all relevant tests in accordance with NICE guidance.
People with COAG, suspected COAG or with OHT are diagnosed and have a management plan formulated by a suitably trained healthcare professional with competencies and experience in accordance with NICE guidance.
People diagnosed with COAG, suspected COAG or with OHT are monitored at intervals according to their risk of progressive loss of vision in accordance with NICE guidance.
People with suspected COAG or with OHT are managed based on estimated risk of conversion to COAG and progression to visual impairment using IOP, CCT and age, in accordance with NICE guidance.
People with COAG, suspected COAG or with OHT have a regular review of management options with their healthcare professional, taking into account comorbidity and other changed circumstances, including a discussion of the benefits and risks of stopping treatment for those at low risk of progressing to visual impairment.
People diagnosed with COAG, suspected COAG or with OHT have access to timely follow-up appointments and specialist investigations at intervals in accordance with NICE guidance. Sufficient capacity is put in place to provide this service, and systems are developed to identify people needing clinical priority if appointments are cancelled, delayed or missed.
Healthcare professionals involved in the care of a person with COAG, suspected COAG or with OHT have appropriate documentation and records available at each clinical encounter in accordance with NICE guidance.
People with COAG who are progressing to loss of vision despite treatment or who present with advanced visual loss are offered surgery with pharmacological augmentation (for example, MMC or 5FU) as indicated and information on the risks and benefits associated with surgery.
People with COAG, suspected COAG or with OHT are given the opportunity to discuss their diagnosis, prognosis and management, and are provided with relevant and accessible information and advice at initial and subsequent visits in accordance with NICE guidance.
People with suspected COAG or with OHT who are not recommended for treatment and whose condition is considered stable are discharged from formal monitoring with a patient-held management plan.
Background information
Definition
What is it?
Glaucoma is a group of eye diseases in which progressive damage to the optic nerve leads to impaired vision and, in a small proportion of people, blindness.
It is characterized by:
Visual field defects — arcuate scotomas, nasal steps, and altitudinal loss.
Changes to the head of the optic nerve — pathological cupping and, as a late sign, pallor of the optic disc.
Nerve fibre layer defects.
The head of the optic nerve is damaged when any combination of the following occur:
Intraocular pressure is abnormally high — the most common cause of damage.
The blood supply to the optic nerve is compromised.
There is a weakness in the optic nerve structure or fibres.
Suspected glaucoma is defined as changes in the optic nerve head (optic disc) or visual field that inconclusively suggest glaucomatous damage (regardless of the intraocular pressure).
Ocular hypertension is a condition defined by consistently or recurrently elevated intraocular pressure (greater than 21 mmHg) and no signs of glaucoma.
[Easty and Sparrow, 1999; Burr et al, 2007; National Collaborating Centre for Acute Care, 2009a]
Anatomy and physiology
What is the anatomy and physiology of the eye relevant to glaucoma?
The descriptions of the anatomy and physiology of the eye may be more easily understood when read in with the aid of a diagram of the eye, such as that on the website of the the Royal National Institute of Blind People (RNIB).
Anterior chamber angle
The space between the iris and pupil behind and the cornea in front is called the anterior chamber.
The anterior chamber angle is the structure formed where the iris and the cornea join the sclera towards the outside of the eye.
The angle becomes narrower in older people.
The width of the angle differs with ethnic background: for example, the width of the angle is narrower in far-Eastern Asian people than in white people.
The angle is narrower in white people who are long-sighted (hypermetropic).
The trabecular meshwork is situated in the anterior chamber angle and functions as the main outflow route for aqueous humour.
Aqueous humour
Aqueous humour is the fluid created by the ciliary body in the posterior chamber, the relatively small fluid-filled space between the lens behind and the iris in front.
Aqueous humour is created mostly by active transport.
Aqueous humour flows out of the eye through the trabecular meshwork (the major pathway) and between the fibres of the ciliary muscle (the minor pathway).
Intraocular pressure
Intraocular pressure keeps the eye in the shape of a globe.
Intraocular pressure is maintained by the balance between production and outflow of aqueous humour.
Raised intraocular pressure can cause glaucoma by damaging the optic nerve.
Intraocular pressure is normally around 10–21 mmHg, but it can be as low as zero in ocular hypotony and as high as 70 mmHg in acute angle closure glaucoma.
Drugs used to treat glaucoma either reduce the production of aqueous humour, or increase its outflow.
Describing glaucoma
How is glaucoma described?
Glaucoma is described in four main ways, according to:
Age of onset: congenital, infantile, juvenile, or adult.
Rate of onset: acute or chronic.
Cause: primary (no known cause), or secondary, with a known cause such as a disease, drug, or developmental condition that increases intraocular pressure and damages the optic nerve.
Mechanism: angle closure glaucoma or open angle glaucoma.
In angle closure glaucoma, the angle between the iris and the cornea is at least partially closed. This blocks the trabecular meshwork and prevents it from draining the intraocular fluid. As intraocular fluid continues to be produced, the pressure within the eye increases and the optic nerve is damaged. The onset may be acute or chronic, and there may be intermittent, prodromal attacks.
In open angle glaucoma, the angle between the iris and the cornea is open. The onset is usually insidious, and the course chronic. It usually affects both eyes, but the signs of damage may be worse in one eye. The intraocular pressure is usually increased but can be within the normal range (normal tension glaucoma).
The National Institute for Health and Clinical Excellence (NICE) guideline regards chronic open angle glaucoma as including both primary chronic open angle glaucoma and glaucoma secondary to pseudoexfoliation or pigment dispersion.
[Easty and Sparrow, 1999; National Collaborating Centre for Acute Care, 2009a]
Causes of secondary glaucoma
What are the more common secondary causes of chronic open angle glaucoma?
Common secondary causes of chronic open angle glaucoma include:
Pseudoexfoliative glaucoma: cellular organelles (pseudoexfoliative material) deposited on the trabecular meshwork restricts outflow of the aqueous humour.
Pigmentary glaucoma: pigment from the back of the iris deposited in the trabecular meshwork (pigment dispersion syndrome) restricts outflow of the aqueous humour.
Neovascular glaucoma: new blood vessels (neovascularization) formed in response to ischaemia (for example with diabetic retinopathy or central retinal vein occlusion) block the outflow of aqueous humour through the trabecular meshwork.
Uveitic glaucoma: in uveitis (inflammation of the uvea: the iris, ciliary body, and choroid plexus), inflammatory cells and proteins block the outflow of aqueous humour through the trabecular meshwork.
Steroid-induced glaucoma: in susceptible people, corticosteroids increase the resistance to outflow of the aqueous humour by affecting transport of aqueous by trabeculocytes in the trabecular meshwork. Raised intraocular pressure induced by corticosteroids is most common with eye drop preparations, but it may develop when corticosteroids are administered by other routes (for example inhaled, skin creams, oral, or intravenous).
Angle-recession glaucoma: trauma to the drainage angle structures reduces outflow of the aqueous humour.
Childhood secondary glaucoma: several uncommon congenital and acquired conditions cause glaucoma in children.
Secondary causes of chronic open angle glaucoma are not further covered in this topic.
[Easty and Sparrow, 1999; National Collaborating Centre for Acute Care, 2009a]
Risk factors for chronic open angle glaucoma
What are the risk factors for chronic open angle glaucoma?
Raised intraocular pressure
Raised intraocular pressure is the main treatable risk factor for chronic open angle glaucoma [NHMRC, 2008].
Age
The prevalence and incidence of chronic open angle glaucoma increase steeply with age.
The prevalence of open angle glaucoma is about 0.3% in people 40 years of age and about 3.3% in people 70 years of age [Burr et al, 2007].
The incidence of open angle glaucoma per 100,000 people per year is about 30 for people 50 years of age and about 181 for people 70 years of age [Burr et al, 2007].
Family history
The risk of chronic open angle glaucoma is increased when a first-degree relative (parent, sibling, child) has glaucoma.
A systematic review found one population-based study [NHMRC, 2008]. The study, conducted in the Netherlands, found the lifetime risk of open angle glaucoma to be 22% in relatives of people with open angle glaucoma, and 2.3% in relatives of controls.
Ethnicity
Chronic open angle glaucoma is more common in people of black African origin than in people of white ethnicity.
A systematic review [Burr et al, 2007] found one study that compared the risk of open angle glaucoma in black Americans and in white Americans. Prevalence rates were four to five times higher in black Americans than white Americans.
A review of glaucoma in sub-Saharan Africa concluded that the highest prevalence is in west Africa [Cook, 2009].
Corticosteroids
The use of oral, inhaled, or high-potency topical corticosteroids has been associated with increased risk of glaucoma [NHMRC, 2008].
Myopia
People who are short-sighted (myopic) are more likely to develop glaucoma and more likely to develop it at a younger age; the risk increases with severity of myopia [NHMRC, 2008].
Diabetes mellitus
A systematic review concluded that diabetes is a risk factor for chronic open angle glaucoma, but some prospective cohort studies provide inconsistent results [NHMRC, 2008].
Prevalence
How common is it?
In the UK, about 500,000 people are estimated to have chronic open angle glaucoma, and around half of these have not been diagnosed [Burr et al, 2007].
Chronic open angle glaucoma is around three to ten times more common than chronic angle closure glaucoma, depending on the population — angle closure glaucoma is more common in Asian people, with the exception of Japanese people [Coleman, 1999; Cedrone et al, 2008].
Prognosis
What is the prognosis?
Ocular hypertension
What is the prognosis for ocular hypertension?
For people with ocular hypertension, the risk of progression to glaucoma depends on the intraocular pressure, the corneal thickness, and their age.
Appropriate treatment reduces the risk of visual loss.
Chronic open angle glaucoma
What is the prognosis for chronic open angle glaucoma?
Without treatment
In most people, chronic open angle glaucoma is asymptomatic until late in its course — visual field defects do not appear until most of the optic nerve fibres have been lost.
As glaucoma progresses, visual losses extend peripherally and centrally.
Peripheral vision is important for moving through a complex or unfamiliar environment, and for detecting movement outside the area of focus. Peripheral vision is therefore necessary for safe driving. Severe loss of the peripheral visual field results in tunnel vision.
Central vision is important for reading, driving, and other activities that require focussed vision.
With treatment
Most people with chronic open angle glaucoma will not go blind, although they will have some visual field defects.
Once vision is lost because of glaucoma, it cannot be restored.
[Spry and Sparrow, 2001; National Collaborating Centre for Acute Care, 2009a]
Acute angle closure glaucoma
What is the prognosis for acute angle closure glaucoma?
Full recovery is likely for people treated promptly for acute angle closure glaucoma.
Irreversible loss of vision after angle closure glaucoma is more likely if there is:
Delay in presenting for treatment.
Delay in reducing intraocular pressure to the normal range.
Inability to maintain intraocular pressure within the normal range.
Complications
What are the complications?
Irreversible loss of vision (partial or complete) is the main complication of glaucoma.
Worldwide, glaucoma is the underlying cause in about 15% of people who are blind [Spry and Sparrow, 2001].
In the UK, glaucoma is mentioned as the cause of blindness in about 13% of registrations. However, as up to 50% of people who are eligible for registration as blind are unregistered, the true figure may be different [Spry and Sparrow, 2001].
Angle closure glaucoma is considerably more likely than open angle glaucoma to cause blindness [Burr et al, 2007].
Diagnosis
Diagnosis of glaucoma and ocular hypertension
Overview of diagnosis
Overview of diagnosis of glaucoma
If a primary healthcare professional suspects chronic open angle glaucoma, they should refer the person non-urgently to an optometrist or ophthalmologist.
If an optometrist finds signs of glaucoma in a person, they should refer the person directly to an consultant ophthalmologist.
An optometrist can make a preliminary diagnosis of glaucoma and, if appropriate, can refer to an ophthalmologist directly or request that a primary healthcare professional makes the referral.
An ophthalmologist should confirm a diagnosis of glaucoma and formulate the management plan.
An optometrist with a specialist glaucoma qualification can diagnose ocular hypertension or suspected glaucoma. Many people with ocular hypertension or suspected chronic open angle glaucoma only require monitoring, and this can be done by community optometrists as part of an enhanced General Ophthalmic Service contract.
If a primary healthcare professional suspects acute angle closure glaucoma they should refer the person immediately to an ophthalmologist to have the diagnosis confirmed and treatment started.
If there is a delay in accessing emergency ophthalmic care, telephone an ophthalmologist for advice on confirming the diagnosis and starting emergency treatment with topical pilocarpine and oral acetazolamide.
If a primary healthcare professional finds that a person is at significantly increased risk of glaucoma, they should advise the person to have their eyes examined regularly by an optometrist (opportunistic targeted testing).
Basis for recommendation
Basis for recommendation
The recommendation to refer people with suspected chronic open angle glaucoma reflects the guideline on chronic open angle glaucoma published by the National Institute for Health and Clinical Excellence (NICE) [National Collaborating Centre for Acute Care, 2009a] and guidelines published by the College of Optometrists and the Royal College of Ophthalmologists [The College of Optometrists and The Royal College of Ophthalmologists, 2009].
The information about referral by optometrists is from a guideline on primary open angle glaucoma from the College of Optometrists, which is based on the NICE guidelines and states, 'refer all 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' [The College of Optometrists, 2009a].
The recommendations on acute angle closure glaucoma are based on the College of Optometrists' clinical management guidelines [The College of Optometrists, 2009b] and on expert reviews [Hoh et al, 2002; Liebmann and Ritch, 2002; Khaw et al, 2004b].
Suspecting acute angle closure glaucoma
When should I suspect acute angle closure glaucoma?
Suspect acute angle closure glaucoma in someone who presents with an acute painful red eye and:
Is female, Asian, long-sighted, or of older age.
Has a history of:
Previous episodes of blurred vision, headaches, or eye pain associated with nausea and seeing halos around lights; these symptoms typically occur in the evening and are relieved by sleeping.
Precipitating factor such as use of an adrenergic drug (for example phenylephrine) or an antimuscarinic drug (for example a tricyclic antidepressant).
Has the following symptoms and signs:
Headache, nausea, and vomiting caused by the painful eye.
Lights are seen surrounded by halos — caused by a hazy oedematous cornea.
Semi-dilated and fixed pupil.
Tender, hard eye.
Impaired visual acuity.
Optic disc is oedematous and hyperaemic, with engorged blood vessels — may be difficult for a non-specialist to detect.
For the clinical features of other causes of acute red eye, see the section on Causes in the CKS topic on Red eye.
Basis for recommendation
Basis for recommendation
CKS based these recommendations on expert opinion in a guideline on primary angle closure glaucoma from the College of Optometrists [The College of Optometrists, 2009b] and a review article [Khaw et al, 2004a].
Suspecting chronic open angle glaucoma
When should I suspect chronic open angle glaucoma?
Chronic open angle glaucoma is most commonly detected by an optometrist finding one or more of the typical features of chronic open angle glaucoma: increased intraocular pressure, visual field defects, and a cupped optic disc.
The optometrist will normally refer the person to a consultant ophthalmologist for confirmation of the diagnosis and initiation of treatment, if necessary.
A GP should suspect chronic open angle glaucoma in someone who presents with loss of part of the visual field without other eye symptoms (which is rare), or when ophthalmoscopy reveals a cupped optic disc in one or both eyes.
People are often not aware that they have a visual field defect, even when it is severe. Pain is typically absent.
Glaucoma is possible if any of the following are present (on expert examination):
The cup is symmetrically enlarged.
The cup-to-disc ratios are different in the two eyes.
The cup is highly asymmetric (usually vertical oval or notched in the neuroretinal rim).
The level of suspicion should be stronger in people with risk factors, such as:
Older age.
Family history of glaucoma in a first-degree relative (parent, sibling, or child).
Black African ethnic ancestry.
If there are clinical signs of chronic open angle glaucoma, refer the person routinely to an optometrist for preliminary confirmation of the diagnosis, and to a consultant ophthalmologist for final confirmation of the diagnosis and formulation of a management plan.
Basis for recommendation
Basis for recommendation
These recommendations reflect the guideline on glaucoma and ocular hypertension published by the National Institute for Health and Clinical Excellence (NICE) [National Collaborating Centre for Acute Care, 2009a].
Presentation of chronic open angle glaucoma
CKS based the information about the clinical presentation of chronic open angle glaucoma on expert reviews [Distelhorst and Hughes, 2003; Khaw et al, 2004a; National Collaborating Centre for Acute Care, 2009a].
Referral to a consultant ophthalmologist
The recommendation that people with chronic open angle glaucoma should be referred to a consultant ophthalmologist for confirmation of the diagnosis is a key priority for implementation in the NICE guideline [National Collaborating Centre for Acute Care, 2009a] and is reflected in guidelines from the College of Optometrists [The College of Optometrists, 2009a].
Opportunistic testing for chronic open angle glaucoma
When would I advise opportunistic testing for chronic open angle glaucoma?
If any of the following risk factors for glaucoma are present, consider opportunistically advising people to have their eyes examined by an optometrist every 2 years, or more frequently if advised by the optometrist.
Older age. People 60 years of age or older should be examined every 2 years until they are 70 years of age, when they should be examined annually — in England free examination is available through the NHS.
Family history of glaucoma. People older than 40 years of age who have a first-degree relative (parent, sibling, or child) with open angle glaucoma should be examined annually — in England free examination is available through the NHS.
Ethnicity. People older than 40 years of age who are of black African origin should be examined annually — in England the NHS eligibility criteria for free eye examinations do not include ethnicity, so these people will need to pay for eye examinations, unless they have a close relative with glaucoma or receive certain social benefits.
People who are at risk of glaucoma and are also socioeconomically deprived should be particularly encouraged to have their eyes examined, because they have a substantially increased risk of presenting late with severe glaucoma.
Basis for recommendation
Basis for recommendation
Systematic screening of the general population for glaucoma
The National Screening Committee (NSC) does not recommend systematic screening of the general population for glaucoma, because a Health Technology Assessment [Burr et al, 2007] found evidence that this would not be cost-effective.
Opportunistic testing of people at high risk of developing glaucoma
A report for the National Screening Committee found that there is no standard approach to detecting glaucoma in the UK and that 'optometrists identify cases of suspected glaucoma by opportunistic case-finding' [Spry and Sparrow, 2001].
Health economic studies are required to inform strategies for testing, because no test or combination of tests can discriminate 100% accurately between people with and without glaucoma [Spry and Sparrow, 2001].
A UK Health Technology Assessment [Burr et al, 2007] provides suggestive evidence that targeted screening of people at high risk of glaucoma:
Is likely to be cost-effective for people with a family history of glaucoma or people of black African ancestry.
Is unlikely to be cost-effective for the general population or people with myopia, diabetes, or other risk factors.
CKS recommends that screening tests should be considered rather than advised, because there are no national guidelines and the evidence of cost-effectiveness is only suggestive.
The specific age groups and retest intervals recommended by CKS are consistent with the economic evidence [Burr et al, 2007], with guidelines for optometrists [The College of Optometrists, 2010], and with NHS policies on providing free sight tests for people older than 60 years of age and for people who have a first-degree relative with glaucoma — these tests are known as the General Ophthalmic Service sight tests.
CKS recommends the same age group and retest intervals for testing people with black African ethnic ancestry as for people with a family history of glaucoma, because these groups have similar risks relative to people with white European ethnicity: 3.80 (95% CI 2.56 to 5.64) and 3.14 (95% CI 2.32 to 4.25), respectively [Burr et al, 2007].
Opportunistic testing on the basis of other risk factors for glaucoma is not recommended, because the prevalence of glaucoma is so low that examination cannot accurately discriminate between people who have it and those who do not have it.
Socioeconomic deprivation and risk of not being examined for glaucoma
A case-control study in England concluded that socioeconomic deprivation was associated with late presentation of glaucoma [Fraser et al, 2001]. Because late presentation increases the risk of subsequent blindness, CKS recommends that socioeconomically deprived people who are at high risk of developing glaucoma be strongly encouraged to have their eyes examined.
Tests for chronic open angle glaucoma
What tests are done to detect chronic open angle glaucoma?
Three types of tests are used to detect glaucoma:
Ophthalmoscopy to assess the optic nerve head.
Tonometry to measure intraocular pressure.
Visual field tests to test for loss of visual field.
Gonioscopy is done to assess the configuration and depth of the peripheral anterior chamber, and to classify the type of glaucoma as open angle, narrow-angle, or angle closure glaucoma.
Central corneal thickness is measured to assess the risks of progression and conversion for people with diagnosed or suspected chronic open angle glaucoma, or ocular hypertension.
Because a variety of technologies are available for each type of test, different services may use different equipment.
Basis for recommendation
Basis for recommendation
The information about the tests used to diagnose people with chronic open angle glaucoma is from a guideline developed by the National Institute for Health and Clinical Evidence (NICE) [National Collaborating Centre for Acute Care, 2009a], which are reflected in guidelines from the College of Optometrists [The College of Optometrists, 2010].
Management
Management
Scenario : Suspected acute angle closure glaucoma - emergency: covers the emergency management in primary care of suspected acute glaucoma when immediate admission is not practical.
Scenario : Chronic open angle glaucoma: describes the primary healthcare professional's role in the shared care management of chronic open angle glaucoma (confirmed or suspected) or ocular hypertension.
Scenario : Suspected acute angle closure glaucoma - emergency
Scenario : Suspected acute angle closure glaucoma - emergency management in primary care
Emergency management in primary care
How should I manage someone with suspected acute angle closure glaucoma?
If acute angle closure glaucoma is suspected, refer immediately for specialist ophthalmology assessment and treatment.
If immediate admission is not possible, start emergency treatment in primary care.
Let the person lie flat with their face up and head not supported by pillows, as this may relieve some of the pressure on the angle.
If the drugs are available, give:
Pilocarpine one drop of 2% in blue eyes or 4% in brown eyes.
Acetazolamide 500 mg orally to reduce production of aqueous humour, provided that there are no contraindications.
Analgesia.
Anti-emetic, if required.
Basis for recommendation
Basis for recommendation
CKS based this information and the recommendations on the College of Optometrists' clinical management guidelines on primary angle closure glaucoma [The College of Optometrists, 2009b] and on expert reviews of the management of acute angle closure glaucoma [Hoh et al, 2002; Liebmann and Ritch, 2002; Khaw et al, 2004b].
Emergency admission for specialist assessment and treatment is required because acute angle closure glaucoma can rapidly cause permanent loss of sight. For more information, see Prognosis for acute angle closure glaucoma.
The College of Optometrists' clinical management guidelines on closed-angle glaucoma recommend for acute angle closure glaucoma:
Commence first-aid treatment with a drop of pilocarpine 2% in blue eyes and pilocarpine 4% in brown eyes, followed by a single dose of oral acetazolamide 500 mg. Then refer the person as an emergency to an ophthalmologist [The College of Optometrists, 2009b].
Emergency management in secondary care
How is acute angle closure glaucoma managed in secondary care?
Initial treatment in secondary care will include topical and intravenous drugs to reduce intra-articular pressure and analgesia. Treatment may be continued in hospital, or with daily visits.
The definitive treatment is surgery to allow aqueous humour to flow from the posterior chamber into the anterior chamber. Usually, this will be laser surgery to create a hole (iridotomy) or shrink the iris away from the trabecular meshwork (iridoplasty) or removal of a small section of iris (peripheral iridectomy). Laser surgery avoids the need for incisions into the eye.
If the cause is a swollen cataractous lens, it may need to be removed.
The unaffected eye is usually also treated preventively with laser surgery, because it is at high risk of acute angle closure glaucoma.
Basis for recommendation
Basis for recommendation
CKS based this information and the recommendations on the College of Optometrists' clinical management guidelines on primary angle closure glaucoma [The College of Optometrists, 2009b] and on expert reviews of the management of acute angle closure glaucoma [Hoh et al, 2002; Liebmann and Ritch, 2002; Khaw et al, 2004b].
Scenario : Chronic open angle glaucoma
Scenario : Chronic open angle glaucoma (confirmed or suspected) or ocular hypertension
Role of primary care
What is the role of primary care in managing chronic open angle glaucoma?
Treatment of confirmed chronic open angle glaucoma, and treatment of ocular hypertension when indicated, are initiated and monitored by specialists.
Ocular hypertension and suspected chronic open angle glaucoma can be diagnosed by qualified optometrists. Most people with these conditions will not require treatment but do need monitoring, which can be done by community optometrists as part of an enhanced service.
Primary care healthcare professionals may be involved in continuing shared care and will need to be aware of:
The information provided in secondary care, driving regulations.
Glaucoma support services and groups.
What to advise people about administering eye drops and compliance aids.
The adverse effects, drug interactions, and safety during pregnancy and breastfeeding of the drugs used to treat glaucoma and ocular hypertension.
Primary care will need to coordinate care with a range of service providers, including optometrists, ophthalmologists, community eye clinics, and social workers.
Basis for recommendation
Basis for recommendation
These recommendations reflect the National Institute for Health and Clinical Excellence (NICE) guideline on the diagnosis and management of chronic open angle glaucoma and ocular hypertension [National Collaborating Centre for Acute Care, 2009a] and take account of guidelines developed by the College of Opticians and by the Royal College of Ophthalmologists [The College of Optometrists, 2009a; The College of Optometrists, 2009d; The College of Optometrists and The Royal College of Ophthalmologists, 2009].
Treatment in secondary care
How are chronic open angle glaucoma (confirmed or suspected) and ocular hypertension treated in secondary care?
For people with ocular hypertension, decisions about whether to start treatment, which drug to prescribe, frequency of monitoring, response to treatment, and when to stop treatment will be made on the basis of the person's age, intraocular pressure, and central corneal thickness.
Many people with ocular hypertension or suspected chronic open angle glaucoma require only monitoring, which can be done by community optometrists as part of an enhanced General Ophthalmic Services contract.
For people who need treatment, the first-line option for people less than 65 years old is a topical beta-blocker. For people at higher risk of developing glaucoma (for example more than 65 years old) a topical prostaglandin analogue (bimatoprost, latanoprost, tafluprost, or travoprost) is recommended.
For early and moderate chronic open angle glaucoma when treatment is indicated, a topical prostaglandin analogue is recommended first line.
For advanced chronic open angle glaucoma, options recommended depend on the person's preference, and are:
Surgery with augmentation — chemotherapy (mitomycin C or 5-fluorouracil) augments surgery by modifying wound healing.
Topical prostaglandin analogues, and other topical intraocular pressure-lowering agents.
Laser treatment (trabeculectomy).
If glaucoma progresses while the person is on drug treatment, or intraocular pressure cannot be reduced sufficiently, the recommended treatment options are:
An alternative class of drug: topical beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic (such as an alpha-2-adrenergic stimulant).
A combination of drug classes.
Surgery with augmentation.
If the person has an allergy to eye drops, the ophthalmologist will stop the eye drops and prescribe the same drug in a preservative-free preparation, prescribe a different drug, or decide that no replacement treatment is required.
Basis for recommendation
Basis for recommendation
These recommendations reflect the National Institute for Health and Clinical Excellence (NICE) guideline on the diagnosis and management of chronic open angle glaucoma and ocular hypertension [National Collaborating Centre for Acute Care, 2009a; National Collaborating Centre for Acute Care, 2009b] and guidelines published by the College of Optometrists [The College of Optometrists, 2009a; The College of Optometrists, 2009c; The College of Optometrists, 2009d; The College of Optometrists and The Royal College of Ophthalmologists, 2009].
NICE based their recommendations on a systematic review of the evidence and on economic analyses, the key findings of which are summarized.
Topical prostaglandin analogues for treating chronic open angle glaucoma
Topical prostaglandin analogues lower intraocular pressure by increasing aqueous outflow.
A systematic review conducted by NICE found:
No relevant placebo-controlled trials of topical prostaglandin analogues.
Evidence from randomized controlled trials (RCTs) that topical prostaglandin analogues are more effective and have a lower risk of serious adverse events than topical beta-blockers.
No studies assessed progression of visual field loss.
Topical prostaglandin analogues were more effective than topical beta-blockers in achieving an acceptable intraocular pressure (moderate-quality evidence).
People using a topical prostaglandin analogue were statistically significantly less likely to experience a respiratory adverse event than people using a topical beta-blocker (moderate-quality evidence).
People using a topical prostaglandin analogue were statistically significantly more likely to develop red eyes than people using a topical beta-blocker (high-quality evidence).
People using a topical prostaglandin analogue had no statistically significant difference in cardiovascular adverse events or an allergic reactions than people using a topical beta-blocker (moderate-quality evidence).
No relevant RCTs that compared topical prostaglandin analogues to topical carbonic anhydrase inhibitors.
Evidence from RCTs that topical prostaglandin analogues are more effective than topical sympathomimetics with respect to reducing intraocular pressure (low-quality evidence).
An economic assessment conducted by NICE found evidence (with minor limitations and direct applicability) that topical prostaglandin analogues are more cost-effective than topical beta-blockers for any stage of chronic open angle glaucoma.
Topical beta-blockers for treating chronic open angle glaucoma
Topical beta-blockers lower intraocular pressure by reducing aqueous production.
A systematic review conducted by NICE found evidence from RCTs that:
Topical beta-blockers in comparison with no treatment reduce intraocular pressure (very low-quality evidence), but it is uncertain whether they reduce the risk of visual field progression (low-quality evidence).
An economic assessment of cost-effectiveness conducted by NICE found evidence (with minor limitations and direct applicability) that:
Topical beta-blockers are more cost effective than no treatment.
Topical carbonic anhydrase inhibitors for treating chronic open angle glaucoma
Topical carbonic anhydrase inhibitors decrease intraocular pressure by reducing aqueous production.
A systematic review conducted by NICE found no relevant RCTs of topical carbonic anhydrase inhibitors for chronic open angle glaucoma. NICE therefore considered the evidence on their use for treating ocular hypertension.
Topical sympathomimetics for treating chronic open angle glaucoma
Topical sympathomimetic drugs lower intraocular pressure by decreasing aqueous production and also increasing aqueous drainage.
A systematic review conducted by NICE found no RCTs that compared a topical sympathomimetic with no treatment.
Topical miotics for treating chronic open angle glaucoma
Topical miotics decrease intraocular pressure by increasing aqueous outflow.
Topical miotics such as pilocarpine are seldom used for chronic open angle glaucoma, because their adverse effects are poorly tolerated.
Patient information
What information should be provided to people diagnosed with chronic open angle glaucoma?
In secondary care, when the diagnosis of chronic open angle glaucoma is confirmed, people should be provided with information, including:
The fact that suspected chronic open angle glaucoma, ocular hypertension, and chronic open angle glaucoma in the early stages cause no symptoms.
Their specific type of glaucoma.
Their options for treatment, and that treatment and monitoring will be required for life.
The importance of the person's role in their own treatment, how to apply eye drops, and the use of compliance aids.
The prognosis for keeping their sight: most people treated for chronic open angle glaucoma will not go blind, but sight cannot be recovered after it has been lost.
Because glaucoma can run in families, family members may wish to be tested for the disease.
The relevant Driver and Vehicle Licensing Agency regulations about driving and glaucoma.
Sources of information and support.
People diagnosed with glaucoma will be provided as required (if they have severe visual loss or poor visual acuity) with a Letter of Vision Impairment, a Referral of Vision Impairment, and a Certificate of Vision Impairment (CVI). The CVI allows the person, should they wish, to register as sight-impaired with their local council.
Basis for recommendation
Basis for recommendation
The information about what information should be provided in secondary care to people diagnosed with chronic open angle glaucoma reflects guidance published by the National Institute for Health and Clinical Excellence (NICE) [National Collaborating Centre for Acute Care, 2009a].
Patient support
What sources of information and support are recommended for people diagnosed with chronic open angle glaucoma?
Information for people with glaucoma is available from:
The Royal National Institute of Blind People (www.rnib.org.uk) provides:
Information and support (including contact details for local support groups) for the visually impaired and for people who have experienced extensive field loss and would benefit from rehabilitation input from a multidisciplinary team.
The International Glaucoma Association information service (www.glaucoma-association.com) provides:
Information about glaucoma.
Information about driving and glaucoma.
The Royal College of Ophthalmologists (www.rcophth.ac.uk) provides:
A booklet on Understanding glaucoma (pdf).
The Eye Health Alliance (www.lookafteryoureyes.org) provides:
Information on general eye health.
Driving and glaucoma
What are the DVLA regulations with respect to driving and glaucoma?
Generally applicable regulations
A driver must have good central visual acuity and adequate peripheral vision while using their glasses or contact lenses if prescribed.
If there are visual field defects in both eyes, the person is legally required to inform the Driver and Vehicle Licensing Agency (DVLA) and to stop driving until a specific test has been performed under the guidance of the DVLA. Advice on informing the DVLA about medical conditions is available online at www.direct.gov.uk.
Because the DVLA updates their regulations on medical standards of fitness to drive every 6 months, the latest version should be checked for changes. Visit www.dft.gov.uk.
Car or motorcycle driving licence holders with glaucoma
If glaucoma causes loss of the visual field in only one eye, the DVLA does not have to be informed provided the person has good vision in the other eye.
If there are visual field defects in both eyes, the person is legally required to inform the DVLA, and to stop driving until a specific test has been performed under the guidance of the DVLA.
Bus, coach, or lorry driving licence holders with glaucoma
If glaucoma affects one or both eyes, the person is legally required to inform the DVLA, and will be required to stop driving if any defect in one eye is not completely compensated for by the other eye.
Basis for recommendation
Basis for recommendation
This information is based on information published by the Driver and Vehicle Licensing Agency (DVLA) on the DVLA and DirectGov websites:
Allergy to eye drops
How do I recognize and manage allergic reactions to anti-glaucoma eye drops?
Allergic reactions are usually due to the preservative in the eye drop but can also be due to the active drug.
Allergic reactions cause the treated eyes and eyelids to itch severely, eyes to become red and injected, and eyelids to become red and swollen. Symptoms and signs become worse after the drops are instilled, and they disappear when treatment is stopped.
If allergy to eye drops is suspected:
Refer to an ophthalmologist, or obtain specialist advice about confirming the suspicion of allergy, withdrawing the eye drops, and further treatment.
Decisions about withdrawing eye drops can require specialist expertise, particularly when disease is severe and more than one type of eye drop is being used.
For people with chronic open angle glaucoma, replacement with a preservative-free preparation is recommended when allergy is confirmed.
For people with ocular hypertension or suspected chronic open angle glaucoma, replacement with a preservative-free preparation is only recommended if they are at high risk of developing chronic open angle glaucoma. If they are not at high risk, treatment is not cost-effective and may be withdrawn.
The risk of progression requires specialist expertise to estimate it from measurements of the intraocular pressure and central corneal thickness.
If the allergic reaction continues despite using a preservative-free preparation, treatment may need to be changed, as the person may be allergic to the active drug.
Basis for recommendation
Basis for recommendation
These recommendations are in line with the National Institute for Health and Clinical Excellence (NICE) guideline on the diagnosis and management of chronic open angle glaucoma and ocular hypertension [National Collaborating Centre for Acute Care, 2009a].
Clinical features of allergy to eye drops
The information about the clinical features of allergy to eye drops is based on an expert review [Khaw et al, 2004b].
Allergic reactions may be due to the active glaucoma drug or to preservative agents used to stabilize the preparation (usually benzalkonium chloride).
Allergy is confirmed if symptoms and signs improve after changing to a preservative-free product or to a different drug.
Referring or obtaining specialist advice when changing medication
CKS recommends that GPs obtain specialist advice or refer people with eye allergy to anti-glaucoma eye drops because:
The decisions may depend on complex risk assessments using information from specialized tests.
Preservative-free eye drops are expensive, may be difficult to obtain, and can be awkward to use.
Management of allergy to eye drops
In the absence of directly applicable clinical and economic evidence, these recommendations are based on indirect evidence from studies using intraocular pressure as an outcome measure [National Collaborating Centre for Acute Care, 2009a].
Promoting adherence
How should I promote adherence to prescribed eye medications for glaucoma?
Ensure that the person or their carer understands how to apply the eye drops. Demonstrate the technique as many times as necessary.
If poor adherence is caused by memory difficulties, consider once-daily or combination products.
If poor adherence is caused by physical problems, recommend a compliance aid (eye drop dispenser) to help position and squeeze the bottle of eye drops.
A list of eye medication products and compatible compliance aids is on the International Glaucoma Association website.
Xal-ease® dispensers are available free from Pfizer for latanoprost products.
Eyot® dispensers are available free from Alcon for travoprost products.
Opticare® and Opticare® Arthro dispensers are prescribable and are compatible with eye drops made by several manufacturers.
Opticare® dispensers are designed for people whose hands shake, or have difficulty placing or squeezing the bottle.
Opticare® Arthro dispensers are designed for people with poor hand grip or limited mobility of the hand or arm. For more information, see the Opticare® website.
Autodrop® dispensers are compatible with a range of eye drop medication, and help ensure that eye drops are accurately delivered to the eye. For more information, visit the Owen Mumford website.
Basis for recommendation
Basis for recommendation
These recommendations reflect the National Institute for Health and Clinical Excellence (NICE) guideline on the diagnosis and management of chronic open angle glaucoma and ocular hypertension [National Collaborating Centre for Acute Care, 2009a].
Advice on administering eye drops
What information and advice should I give people using eye drops for glaucoma?
Advise people using eye drops to:
Wash their hands before and after using their eye drops.
Remove soft contact lenses before applying eye drops and wait at least 15 minutes before reinserting them.
Shake the bottle of eye drops before each use.
Minimize systemic absorption and adverse effects by closing their eyes after administering eye drops, gently but firmly pressing the tear duct against the nose for at least 1 minute, and then removing excess solution with absorbent tissue.
Note the date on which each eye preparation is opened, as it should be replaced after 4 weeks.
Ensure that the eye preparations are stored according to the manufacturer's instructions.
Most eye drops should be stored at room temperature, in a cool, dry place and away from direct sunlight and heat.
Latanoprost (Xalatan® and Xalacom®) should be stored in a refrigerator before opening. Once opened, they can be kept in a cool place for up to 4 weeks.
Cool wallets and insulation pouches designed to be used in warmer climates can store eye drops for up to 48 hours without the need of a fridge. For more information, visit the International Glaucoma Association's website.
Advise people who are using more than one type of eye drop to:
Allow at least 5 minutes between using different eye preparations to avoid wash-out.
Use simple aqueous solutions before gels or suspensions, and to use ointments last.
Basis for recommendation
Basis for recommendation
Storage of latanoprost
The recommendation on the storage of latanoprost is based on manufacturers' Summaries of Product Characteristics [ABPI Medicines Compendium, 2009a; ABPI Medicines Compendium, 2010g].
Removing contact lenses before applying eye drops
The recommendation on removing contact lenses is based on the manufacturer's Summary of Product Characteristics [ABPI Medicines Compendium, 2009a], and the British National Formulary [BNF 59, 2010].
Many eye drops contain benzalkonium chloride as preservative, which is absorbed by soft contact lenses [ABPI Medicines Compendium, 2009a].
Some drugs and preservatives can accumulate in soft lenses and may induce toxic reactions [BNF 59, 2010].
Important aspects of prescribing information relevant to primary healthcare are covered in this section specifically for the drugs recommended in this CKS topic. For further information on contraindications, cautions, drug interactions, and adverse effects, see the electronic Medicines Compendium (eMC) (http://medicines.org.uk/emc), or the British National Formulary (BNF) (www.bnf.org).
Topical prostaglandin analogues
Topical prostaglandin analogues
Action
How do topical prostaglandin analogues work?
Topical prostaglandin analogues reduce intraocular pressure by increasing uveoscleral outflow and hence increasing the outflow of aqueous humour.
Basis for recommendation
This information is based on a guideline on the diagnosis and management of chronic open angle glaucoma and ocular hypertension from the National Institute for Health and Clinical Excellence (NICE) [NICE, 2009] and expert review articles [Khaw et al, 2004b; Weinreb and Khaw, 2004].
Availablilty
Which topical prostaglandin analogues are available in the UK for the treatment of glaucoma?
Topical prostaglandin analogues available in the UK for the treatment of glaucoma are:
Latanoprost 50 micrograms/mL drops.
Travoprost 40 micrograms/mL drops.
Bimatoprost 100 micrograms/mL and 300 mcg/mL drops.
Tafluprost 15 micrograms/mL unit dose drops (preservative free).
Topical prostaglandin analogues are also available as combination preparations containing timolol 0.5%. These preparations are:
Bimatoprost and timolol — Ganfort®.
Latanoprost and timolol — Xalacom®.
Travoprost and timolol — DuoTrav®.
Basis for recommendation
This information is from the British National Formulary [BNF 59, 2010].
Adverse effects
What key adverse effects are associated with topical prostaglandin analogues?
Local adverse effects include:
Increased brown pigmentation in the iris of the treated eye; this is especially noticeable when the iris is mixed-coloured (blue–brown, grey–brown, yellow–brown, or green–brown).
Increased pigmentation of peri-ocular skin.
Darkening, thickening, and lengthening of the eyelashes.
Blepharitis.
Ocular pain and irritation.
Conjunctival hyperaemia.
Dry eyes.
Eyelid oedema and rash, keratitis, blurred vision, and conjunctivitis have also been rarely reported.
Allergic reaction to the active drug or preservative.
Systemic adverse effects are rare. However, the following have been reported:
Dyspnoea.
Exacerbation of asthma.
Dizziness.
Arthralgia.
Myalgia.
Iritis.
Uveitis.
Headache.
Photophobia.
Basis for recommendation
This information is from published data from the manufacturers' Summaries of Product Characteristics [ABPI Medicines Compendium, 2007; ABPI Medicines Compendium, 2009a], the textbook Martindale: the complete drug reference [Sweetman, 2009], and the British National Formulary [BNF 59, 2010].
Doses
How are topical prostaglandin analogues typically prescribed for the treatment of glaucoma?
Bimatoprost, latanoprost, and travoprost — one drop once daily, preferably in the evening.
Ganfort® (bimatoprost with timolol) — one drop once daily, preferably in the morning.
Duotrav® (travoprost with timolol) — one drop once daily, preferably in the evening.
Xalacom® (latanoprost with timolol) — one drop once daily.
Topical prostaglandin analogues are not licensed for children under 18 years of age.
Basis for recommendation
This information is from the manufacturers' Summaries of Product Characteristics [ABPI Medicines Compendium, 2007; ABPI Medicines Compendium, 2009a; ABPI Medicines Compendium, 2009d; ABPI Medicines Compendium, 2010g; ABPI Medicines Compendium, 2010b] and the British National Formulary [BNF 59, 2010].
Interactions
What drug interactions are important with topical prostaglandin analogues?
There are no important common drug-drug interactions with topical prostaglandin analogues. However, the concurrent use of two or more topical prostaglandin analogues or derivatives is not recommended.
Basis for recommendation
This information is taken from the textbook Stockley's drug interactions [Baxter, 2008] and the manufacturer's Summary of Product Characteristics [ABPI Medicines Compendium, 2009a].
There are reports of elevations in intraocular pressure after the concomitant use of two prostaglandin analogues [ABPI Medicines Compendium, 2009a].
Topical beta-blockers
Topical beta-blockers
Action
How do topical beta-blockers work?
Topical beta-blockers reduce intraocular pressure by decreasing the rate of production of aqueous humour.
Oral beta-blockers also reduce intraocular pressure, but they are not used primarily to treat or prevent glaucoma because of the risk of systemic adverse effects.
Basis for recommendation
This information is based on a guideline on the diagnosis and management of chronic open angle glaucoma and ocular hypertension from the National Institute for Health and Clinical Excellence (NICE) [NICE, 2009], expert review articles [Khaw et al, 2004b; Weinreb and Khaw, 2004], and the British National Formulary [BNF 59, 2010].
Availablilty
Which topical beta-blockers are available in the UK for the treatment of glaucoma?
Topical beta-blocker eye drops available in the UK for the treatment of glaucoma are:
Betaxolol hydrochloride 0.5% solution, 0.25% suspension, and 0.25% modified release unit dose eye drop suspension (preservative free).
Carteolol hydrochloride 1% and 2% drops.
Levobunolol hydrochloride 0.5% drops and 0.5% unit dose eye drops (preservative free).
Metipranolol 0.1% Minims® (preservative-free, single-use application packs).
Timolol maleate 0.25% and 0.5% drops and 0.25% and 0.5% unit dose eye drops (preservative free).
Timolol maleate is also available as:
Long-acting once daily preparations — Nyogel® (0.1% eye gel) and Timoptol®-LA (0.25% and 0.5% ophthalmic gel-forming solution).
Combination preparations containing prostaglandin analogues, sympathomimetics, or carbonic anhydrase inhibitors.
Combination preparations containing timolol
With prostaglandin analogues:
Bimatoprost — Ganfort®
Latanoprost — Xalacom®
Travoprost — DuoTrav®
With sympathomimetics:
Brimonidine — Combigan®
With carbonic anhydrase inhibitors:
Brinzolomide — Azarga®
Dorzolamide — Cosopt® (also available as preservative-free formulation)
Basis for recommendation
This information is from the British National Formulary [BNF 59, 2010].
Doses
How are topical beta-blockers typically prescribed for the treatment of glaucoma?
Betaxolol and carteolol — one drop in the affected eye twice daily.
Levobunolol hydrochloride — one drop in the affected eye once or twice daily.
Metipranolol — one drop in the affected eye twice daily.
Timolol maleate — one drop (0.25%) in the affected eye twice daily. However, if clinical response is not adequate, increase to one drop 0.5% twice a day.
The long-acting timolol preparations (Nyogel® and Timoptol®-LA) are applied once daily.
Topical beta-blockers are not currently licensed for use in children younger than 18 years of age.
Basis for recommendation
This information is from the manufacturers' Summaries of Product Characteristics [ABPI Medicines Compendium, 2003; ABPI Medicines Compendium, 2008a; ABPI Medicines Compendium, 2008b; ABPI Medicines Compendium, 2009b] and the British National Formulary [BNF 59, 2010].
Adverse effects
What key adverse effects are associated with topical beta-blockers?
Local adverse effects
Local adverse effects are common and include burning, stinging, pain, itching, redness, dry eyes, and allergic reactions to the active drug or preservatives.
Less common local adverse effects are blepharoconjunctivitis and corneal disorders.
Systemic adverse effects
Systemic adverse effects may occur, especially when high doses are prescribed for prolonged periods. These include:
Bradycardia.
Bronchoconstriction.
Worsening of severe peripheral and central circulatory disorders.
Sleep disturbances.
Hallucination.
Depression.
Fatigue.
Loss of libido.
Basis for recommendation
This information is from the textbook Martindale: the complete drug reference [Sweetman, 2009] and the British National Formulary [BNF 59, 2010].
Interactions
What drug interactions are important with topical beta-blockers?
Systemic absorption may follow topical application and could lead to the following interactions:
Systemic beta-blockers — monitor concurrent use. Concurrent use of a topical beta-blocker with a systemic beta-blocker may exaggerate the effects of beta-blockers, such as hypotension or bradycardia. It may also exaggerate the effect on intraocular pressure.
Calcium-channel blockers, such as verapamil — avoid concurrent use. Concurrent use of topical beta-blocker and verapamil can lead to bradycardia, asystole, or sinus arrest.
Flecainide — monitor for bradycardia. Bradycardia has been reported in people taking flecainide and using timolol eye drops.
Basis for recommendation
This information is from the textbook Stockley's drug interactions [Baxter, 2008], the manufacturers' Summaries of Product Characteristics [ABPI Medicines Compendium, 2008a; ABPI Medicines Compendium, 2008b; ABPI Medicines Compendium, 2009b], and the British National Formulary [BNF 59, 2010].
Topical sympathomimetics
Topical sympathomimetics
Action
How do topical sympathomimetics work?
Topical sympathomimetics reduce intraocular pressure by decreasing aqueous production and increasing aqueous drainage.
Basis for recommendation
This information is based on a guideline on the diagnosis and management of chronic open angle glaucoma and ocular hypertension from the National Institute for Health and Clinical Excellence (NICE) [NICE, 2009].
Availability
Which topical sympathomimetics are available in the UK for the treatment of glaucoma?
Topical sympathomimetics available in the UK for the treatment of glaucoma are:
Brimonidine tartrate 0.2% drops.
Dipivefrine hydrochloride 0.1% eye drops.
Brimonidine tartrate is also available as Combigan®, a compound preparation containing timolol 0.5%.
Basis for recommendation
This information is from the British National Formulary [BNF 59, 2010].
Doses
How are topical sympathomimetics typically prescribed in secondary care for the treatment of glaucoma?
Brimonidine and dipivefrine — one drop in affected eyes twice daily, approximately 12 hours apart.
Combigan® (brimonidine tartrate 0.2% and timolol 0.5%) — one drop twice daily.
No dosage adjustment is required for elderly patients.
Basis for recommendation
This information is from the manufacturers' Summaries of Product Characteristics [ABPI Medicines Compendium, 2008c; ABPI Medicines Compendium, 2008d] and the British National Formulary [BNF 59, 2010].
Adverse effects
What key adverse effects are associated with topical sympathomimetics?
Local adverse effects include:
Hyperaemia, burning, and stinging of the eyes.
Dry mouth and abnormal taste in the mouth, which are associated with drainage of the drug into the nasopharynx.
Allergic reaction to the active drug or preservative.
Systemic adverse effects are rare. However, headaches, drowsiness, dizziness, and gastro-intestinal symptoms have been reported.
Basis for recommendation
This information is from the textbook Martindale: the complete drug reference [Sweetman, 2009] and the British National Formulary [BNF 59, 2010].
Interactions
What drug interactions are important with topical sympathomimetics?
Central nervous system (CNS) depressants — monitor closely when topical sympathomimetics are used with CNS depressants, such as alcohol, barbiturates, opiates, sedatives, or anaesthetics.
CNS depressants could potentiate the effects of topical sympathomimetics.
Basis for recommendation
This information is from the textbook Stockley's drug interactions [Baxter, 2008].
Carbonic anhydrase inhibitors
Carbonic anhydrase inhibitors
Action
How do carbonic anhydrase inhibitors work?
Carbonic anhydrase inhibitors reduce intraocular pressure by reducing the secretion of aqueous humour.
Basis for recommendation
This information is based on a guideline on the diagnosis and management of chronic open angle glaucoma and ocular hypertension from the National Institute for Health and Clinical Excellence (NICE) [NICE, 2009], expert review articles [Khaw et al, 2004b; Weinreb and Khaw, 2004], and the British National Formulary [BNF 59, 2010].
Availability
Which carbonic anhydrase inhibitors are available in the UK for the treatment of glaucoma?
Topical
Brinzolamide 10 mg/mL drops.
Dorzolamide hydrochloride 2% eye drops and 2% unit dose eye drops (preservative free).
Brinzolamide and timolol 0.5% — Azarga® ophthalmic suspension.
Dorzolamide and timolol 0.5% — Cosopt® ophthalmic solution and unit dose eye drops.
Oral
Acetazolamide 250 mg tablets and 250 mg slow-release capsules (Diamox® SR).
Parenteral
Acetazolamide is also available as an injection for intravenous administration.
Basis for recommendation
This information is from the British National Formulary [BNF 59, 2010].
Adverse effects
What key adverse effects are associated with carbonic anhydrase inhibitors?
Topical carbonic anhydrase inhibitors
What key adverse effects are associated with topical carbonic anhydrase inhibitors?
Local adverse effects include:
Blepharitis.
Eye irritation, pain, and dryness.
Blurred vision.
Lacrimation.
Allergic reaction to the active drug or preservatives.
Systemic adverse effects are uncommon but can include:
Headache.
Drowsiness.
Dizziness.
Gastro-intestinal symptoms, such as nausea, vomiting, and dyspepsia.
Dry mouth and taste disturbances (associated with drainage of the drops into the nasopharynx).
Stevens–Johnson syndrome.
Basis for recommendation
This information is from the textbook Martindale: the complete drug reference [Sweetman, 2009] and the British National Formulary [BNF 59, 2010].
Oral carbonic anhydrase inhibitors
What key adverse effects are associated with oral carbonic anhydrase inhibitors?
Adverse reactions during short-term use are usually non-serious and include:
Tingling feeling in the extremities.
Loss of appetite or taste disturbance.
Weight loss.
Nausea, vomiting, and diarrhoea.
Polyuria.
Flushing.
Thirst.
Headache.
Dizziness.
Fatigue.
Irritability.
Depression.
Kidney stones.
Stevens–Johnson syndrome.
Reduced libido.
Drowsiness and confusion.
Rarely, photosensitivity has been reported.
Allergic reaction, including cross-reactivity with sulphonamide antibiotics.
Basis for recommendation
This information is from the manufacturers' Summaries of Product Characteristics and the British National Formulary [BNF 59, 2010].
Doses
How are carbonic anhydrase inhibitors typically prescribed in secondary care for the treatment of glaucoma?
Topical
Brinzolamide — one drop twice daily, increased to three times daily if necessary.
Azarga® (brinzolamide and timolol) — one drop twice daily.
Dorzolamide — one drop three times daily (with topical beta-blockers, apply twice daily).
Cosopt® (dorzolamide with timolol) — one drop twice daily.
Oral
Acetazolamide — 0.25 g to 1 g daily in divided doses.
Basis for recommendation
This information is from the manufacturers' Summaries of Product Characteristics [ABPI Medicines Compendium, 2008e; ABPI Medicines Compendium, 2010a] and the British National Formulary [BNF 59, 2010].
Interactions
What drug interactions are important with carbonic anhydrase inhibitors?
Topical carbonic anhydrase inhibitors
What drug interactions are important with topical carbonic anhydrase inhibitors?
There are no common important drug interactions with topical carbonic anhydrase inhibitors.
Basis for recommendation
This information is taken from the textbook Stockley's drug interactions [Baxter, 2008] and the manufacturers' Summaries of Product Characteristics [ABPI Medicines Compendium, 2008e; ABPI Medicines Compendium, 2010a].
In clinical studies, dorzolamide was used safely with the following drugs [Baxter, 2008]:
Timolol ophthalmic solution.
Betaxolol ophthalmic solution.
Angiotensin-converting enzyme (ACE) inhibitors.
Calcium channel blockers.
Diuretics.
Nonsteroidal anti-inflammatory drugs, including aspirin.
Hormones, such as oestrogen, insulin, and thyroxine.
Oral carbonic anhydrase inhibitors
What drug interactions are important with oral carbonic anhydrase inhibitors?
Aspirin — avoid concomitant use with high-dose aspirin and consider prescribing paracetamol or a nonsteroidal anti-inflammatory drug, such as ibuprofen. If indicated, monitor for signs of toxicity, such as confusion, lethargy, hyperventilation, and tinnitus.
Concomitant use of acetazolamide and high-dose aspirin can result in metabolic acidosis.
Anticonvulsants, such as phenytoin, carbamazepine, and phenobarbital — monitor concomitant administration, as acetazolamide can modify the metabolism of some anticonvulsants.
Carbamazepine — monitor for signs of carbamazepine toxicity, such as nausea, vomiting, ataxia, and drowsiness. Acetazolamide can cause an increase in serum carbamazepine levels.
Phenobarbital, phenytoin, and primidone — severe osteomalacia and rickets have been reported in a few people taking phenobarbital, phenytoin, or primidone with acetazolamide.
Ciclosporin — monitor ciclosporin levels and effects routinely, especially when acetazolamide is initiated or stopped.
Acetazolamide can cause a marked and rapid increase in serum ciclosporin levels (up to six-fold in 72 hours). This may be accompanied by renal toxicity.
Lithium — monitor concurrent administration.
Acetazolamide increases lithium excretion and may lead to decreased lithium levels.
Quinidine — monitor the effects of quinidine if acetazolamide is stopped, and adjust as necessary. Consider monitoring potassium levels to ensure its within the normal range.
Acetazolamide can cause a large increase in urinary pH, leading to quinidine retention and toxicity. Acetazolamide can rarely cause hypokalaemia, which can increase the toxicity of QT-prolonging drugs, such as quinidine.
Other carbonic anhydrase inhibitors — avoid concomitant use because of possible additive effects.
Basis for recommendation
This information is taken from the textbook Stockley's drug interactions [Baxter, 2008] and the manufacturer's Summary of Product Characteristics [ABPI Medicines Compendium, 2010f].
Contraindications
What contraindications are important when prescribing acetazolamide?
Acetazolamide should not be used in people with:
Hypokalaemia.
Hyponatraemia.
Severe kidney and liver disease or dysfunction.
Adrenal gland failure.
Hyperchloremic acidosis.
Hepatic cirrhosis.
Hypersensitivity to sulphonamides.
Chronic non-congestive angle closure glaucoma (long-term use is contraindicated).
Basis for recommendation
This information is from the manufacturer's Summary of Product Characteristics [ABPI Medicines Compendium, 2010f].
Hepatic cirrhosis
Acetazolamide (Diamox®) should not be used in patients with hepatic cirrhosis, as this may increase the risk of hepatic encephalopathy.
Chronic non-congestive angle closure glaucoma
Long-term use of acetazolamide may permit organic closure of the angle to occur while the worsening glaucoma is masked by decreased intraocular pressure.
Hypersensitivity to sulphonamides
Acetazolamide is a sulphonamide derivative.
Topical miotics
Topical miotics
Action
How do topical miotics work?
Topical miotics work by increasing the flow of aqueous humour from the eye, resulting in a decrease in intraocular pressure.
Basis for recommendation
This information is from a guideline on the diagnosis and management of chronic open angle glaucoma and ocular hypertension from the National Institute for Health and Clinical Excellence (NICE) [NICE, 2009] and the manufacturer's Summary of Product Characteristics [ABPI Medicines Compendium, 2008f].
Availability
Which topical miotics are licensed in the UK for the treatment of glaucoma?
The only topical miotic licensed in the UK for the treatment of glaucoma is pilocarpine hydrochloride.
Pilocarpine hydrochloride is available as:
Pilocarpine hydrochloride 0.5%, 1%, 2%, 3%, and 4% drops.
Pilocarpine nitrate 2% (Minims® — preservative-free, single-use application packs).
Pilocarpine hydrochloride 4% long-acting ophthalmic gel (Pilogel®).
Basis for recommendation
This information is from the British National Formulary [BNF 59, 2010].
Doses
How are topical miotics typically prescribed in secondary care for the treatment of glaucoma?
Pilocarpine — one drop up to four times daily.
Pilogel® (long-acting pilocarpine preparation) — one drop once daily at bedtime.
Basis for recommendation
This information is from the manufacturer's Summary of Product Characteristics [ABPI Medicines Compendium, 2008f] and the British National Formulary [BNF 59, 2010].
Adverse effects
What key adverse effects are associated with topical miotics?
Local adverse effects of pilocarpine eye drops include:
Burning, itching, lacrimation, and smarting.
Brow ache, loss of accommodation, and blurred vision.
Conjunctival vascular congestion.
Myopia.
Vitreous haemorrhage and pupillary block.
Lens changes have also been reported with long-term use.
Allergic reaction to the active drug or preservative.
Retinal detachment.
Systemic adverse effects are rare at normal doses. However, when high doses are given (for example in the treatment of acute angle closure glaucoma), the risks of systemic adverse effects are increased.
Systemic adverse effects may include hypotension, bradycardia, bronchial spasm, pulmonary oedema, salivation, sweating, nausea, vomiting, headache, and diarrhoea.
Basis for recommendation
This information is from the manufacturer's Summary of Product Characteristics [ABPI Medicines Compendium, 2008f], the textbook Martindale: the complete drug reference [Sweetman, 2009], and the British National Formulary [BNF 59, 2010].
Interactions
What drug interactions are important with topical miotics?
There are no important common drug interactions with pilocarpine eye drops.
Basis for recommendation
This information is from the manufacturer's Summary of Product Characteristics [ABPI Medicines Compendium, 2008f].
Preservative free formulations
Which anti-glaucoma drugs are available as preservative-free formulations?
The following anti-glaucoma drugs are available as preservative-free formulation:
Prostaglandin analogues
Tafluprost 15 microgram/mL unit dose drops (Saflutan®).
Beta-blockers
Betaxolol hydrochloride 0.25% modified release unit dose eye drop suspension (Betopic®).
Levobunolol hydrochloride 0.5% unit dose eye drops (Betagan®).
Metipranolol 0.1% (Minims®).
Timolol maleate 0.25% and 0.5% unit dose eye drops (Timoptol®).
Sympathomimetics
There are no preservative-free topical sympathomimetics.
Carbonic anhydrase inhibitors
Dorzolamide hydrochloride 2% unit dose eye drops.
Cosopt® (dorzolamide and timolol) unit dose eye drops.
Miotics
Pilocarpine nitrate 2% (Minims®).
Basis for recommendation
This information is from the British National Formulary [BNF 59, 2010].
Combination preparations
Which anti-glaucoma drugs are available as combination preparations?
The following anti-glaucoma drugs are available as combination preparations containing timolol 0.5%:
Prostaglandin analogues
Bimatoprost and timolol — Ganfort® eye drops.
Latanoprost and timolol — Xalacom® eye drops.
Travoprost and timolol — DuoTrav® eye drops.
Sympathomimetics
Brimonidine and timolol — Combigan® eye drops.
Carbonic anhydrase inhibitors
Brinzolamide and timolol — Azarga® ophthalmic suspension.
Dorzolamide and timolol — Cosopt® ophthalmic solution and unit dose eye drops.
Basis for recommendation
This information is from the British National Formulary [BNF 59, 2010].
Pregnancy and breastfeeding
Should anti-glaucoma drugs be used by pregnant or breastfeeding women?
Anti-glaucoma eye drops
Should anti-glaucoma eye drops be used by pregnant or breastfeeding women?
Glaucoma in woman of reproductive age is rare.
If a woman using topical anti-glaucoma drugs becomes pregnant, seek specialist advice.
Anti-glaucoma drugs are used during pregnancy and breastfeeding, but under the close supervision of a specialist.
Pregnant or breastfeeding women on anti-glaucoma medications should be advised to place pressure over the tear duct by the corner of the eye (punctal occlusion) for one minute or more after instillation of the drops, then remove the excess solution with an absorbent tissue in order to minimize systemic absorption.
Basis for recommendation
Topical prostaglandin analogues
The manufacturers of latanoprost, travoprost, tafluprost, and bimatoprost do not recommend their use in pregnancy or breastfeeding, as their safety for use in human pregnancies have not been studied and they may have pharmacological effects on the pregnancy or the fetus [ABPI Medicines Compendium, 2007; ABPI Medicines Compendium, 2009a; ABPI Medicines Compendium, 2010c; ABPI Medicines Compendium, 2010d; ABPI Medicines Compendium, 2010e].
A pharmaceutical database of drugs used during breastfeeding suggests that topical prostaglandin analogues can be used [LactMed, 2009a; LactMed, 2009b; LactMed, 2009c].
Owing to their short half-life, topical prostaglandin analogues are unlikely to reach the bloodstream of the infant or cause any adverse effects in breastfed infants. However, to reduce the amount of drug that reaches the breast milk, the mother should be advised to practice punctal occlusion after instillation of the drops.
Topical beta-blockers
The manufacturers of betaxolol, metipranolol, timolol, and levobunolol do not recommend their use in pregnancy and breastfeeding owing to the lack of human data [ABPI Medicines Compendium, 2003; ABPI Medicines Compendium, 2008a; ABPI Medicines Compendium, 2008b; ABPI Medicines Compendium, 2009b ].
The amount of topical beta-blockers present in breast milk is too small to harm the infant. However, the infant should be monitored for possible toxicity due to beta-blockade [Schaefer et al, 2007].
Topical sympathomimetics
The manufacturers of brimonidine and dipivefrine recommend that they are used in pregnancy only if the benefits outweigh the potential risks [ABPI Medicines Compendium, 2008c; ABPI Medicines Compendium, 2008d].
The manufacturers of brimonidine and dipivefrine do not recommend their use by breastfeeding women [ABPI Medicines Compendium, 2008c; ABPI Medicines Compendium, 2008d].
Topical carbonic anhydrase inhibitors
The manufacturers of brinzolamide and dorzolamide do not recommend that they be used in pregnancy or breastfeeding because human studies are lacking [ABPI Medicines Compendium, 2008e; ABPI Medicines Compendium, 2010a].
Topical miotics
The manufacturers of Pilogel® recommend that it should be used in pregnancy only if it is considered essential [ABPI Medicines Compendium, 2009c].
The textbook Drugs during pregnancy and lactation [Schaefer et al, 2007] states that there have been no reports of serious adverse effects for the unborn child when pregnant women have been treated with pilocarpine.
The manufacturers of Pilogel® recommend that it can be used cautiously in breastfeeding because it may be excreted in breast milk [ABPI Medicines Compendium, 2009c].
An expert review article [Bennett and Bennett, 1996] and a pharmaceutical database of drugs used during breastfeeding [LactMed, 2009d] suggest that pilocarpine can be safely used by breastfeeding women, although the evidence of use is limited.
Acetazolamide
Should acetazolamide be used by pregnant or breastfeeding women?
Glaucoma in women of reproductive age is rare.
If a woman using acetazolamide becomes pregnant, seek specialist advice.
Limited data suggests that acetazolamide is not associated with increased risk of congenital malformation.
Acetazolamide can be used by breastfeeding women. However, extreme caution should be exercised and the infant should be monitored for signs of toxicity.
Basis for recommendation
Pregnancy
The manufacturer does not recommend use of acetazolamide in pregnancy because safety in human pregnancies has not been studied [ABPI Medicines Compendium, 2010f].
However, the UK Teratology Information Service have found limited data on the effects of acetazolamide in human pregnancy which do not indicate that it is associated with an increased risk of congenital malformations compared with the background incidence of 2–3% [NTIS, 2006].
Breastfeeding
A pharmaceutical database of drugs used during breastfeeding suggests that acetazolamide can be used in women who are breastfeeding [LactMed, 2009e].
Limited information indicates that maternal doses of acetazolamide up to 1000 mg daily produce low levels in milk and would not be expected to cause any adverse effects in breastfed infants.
It is unlikely that acetazolamide will lead to any harmful effects in infants. However, extreme caution should be exercised when administering to breastfeeding women [ABPI Medicines Compendium, 2010f].
Evidence
Evidence
Supporting evidence
This section summarizes the evidence supporting decisions about screening that will be made by generalists in primary care.
Evidence on management decisions that are made by specialists or in secondary care is outside the scope of this topic and is available in the full guideline (and its appendices) Glaucoma: diagnosis and management of chronic open angle glaucoma and ocular hypertension published by the National Institute for Health and Clinical Excellence (NICE) [National Collaborating Centre for Acute Care, 2009a; National Collaborating Centre for Acute Care, 2009b].
Screening
Evidence on screening for glaucoma
Evidence from a Health Technology Assessment (HTA) which conducted a systematic review and developed an economic model suggests, with some uncertainty, that screening of the general population for open angle glaucoma would not be cost-effective, but that screening might be cost-effective for people of black African origin or those with a family history of glaucoma.
The HTA programme of the UK National Institute for Health Research (NIHR) commissioned an HTA of screening for glaucoma [Burr et al, 2007].
The main objective of the HTA was to model for the UK estimates of cost and cost-effectiveness of screening for open angle glaucoma.
The authors conducted systematic reviews to provide evidence-based estimates for the parameters of the economic model. The authors consulted widely when deciding on the screening strategies to assess.
The key results of the HTA were:
No randomized controlled trials (RCTs) of screening strategies were found.
No potential screening test was clearly more accurate than any other, but for each test there were only few, heterogenous studies.
Most potential screening tests reviewed had an estimated specificity of 85% or higher. No test was clearly most accurate, with only a few, heterogeneous studies for each test.
Two RCTs provided evidence that the risk of progression of eye damage is reduced by early treatment. For the economic model, it was estimated from this evidence that the average time to become blind in at least one eye would be about 23 years without treatment and about 35 years with treatment.
For screening to be cost-effective, the prevalence of open angle glaucoma needed to be above about 4%.
Screening was found to be cost-effective for people of black African origin or those with a family history of open angle glaucoma.
Screening was found to be not cost-effective for the general population of any age group or for people with other risk factors, such as myopia and diabetes.
The authors warned that there is considerable uncertainty in the predictions of the economic model. In particular, screening would be cost-effective if the actual rates of progression or costs of being visually impaired are higher than the estimates used in the model.
Search strategy
Scope of search
A literature search was conducted for guidelines, systematic reviews and randomized controlled trials on primary care management of glaucoma, with additional searches for systematic reviews and RCTs in the following area:
Pharmacological treatment of glaucoma
Search dates
January 2006 – May 2010 for evidence-based guidelines, systematic reviews, RCTs on glaucoma management in general.
January 2009 – May 2010 for systematic reviews and RCTs on pharmacological treatment of glaucoma.
Key search terms
Various combinations of searches were carried out. The terms listed below are the core search terms that were used for Medline and these were adapted for other databases. Further details are available on request.
exp Glaucoma, Angle-Closure/, exp Glaucoma, Open-Angle/, exp Glaucoma/, exp Ocular Hypertension/
Table 1. Key to search terms.| Search commands | Explanation |
|---|---|
| / | indicates a MeSh subject heading with all subheadings selected |
| .tw | indicates a search for a term in the title or abstract |
| exp | indicates that the MeSH subject heading was exploded to include the narrower, more specific terms beneath it in the MeSH tree |
| $ | indicates that the search term was truncated (e.g. wart$ searches for wart and warts) |
Topic specific literature search sources
The Royal College of Ophthalmologists
The Do Once and Share (DOAS) Glaucoma Project
American Academy of Ophthalmology
The British & Irish Orthoptic Society
Canadian Ophthalmological Society
Sources of guidelines
National Institute for Health and Clinical Excellence (NICE)
Scottish Intercollegiate Guidelines Network (SIGN)
National Guidelines Clearinghouse
British Columbia Medical Association
Institute for Clinical Systems Improvement
Guidelines International Network
National Library of Guidelines
National Health and Medical Research Council (Australia)
University of Michigan Medical School
Michigan Quality Improvement Consortium
Royal Australian College of General Practitioners
National Resource for Infection Control
NHS Scotland National Patient Pathways
Agency for Healthcare Research and Quality
UK Ambulance Service Clinical Practice Guidelines
RefHELP NHS Lothian Referral Guidelines
Medline (with guideline filter)
Driver and Vehicle Licensing Agency
NHS Plus (occupational health practice)
Sources of systematic reviews and meta-analyses
Systematic reviews
Protocols
Database of Abstracts of Reviews of Effects
Medline (with systematic review filter)
EMBASE (with systematic review filter)
Sources of health technology assessments and economic appraisals
NIHR Health Technology Assessment programme
NHS Economic Evaluations
Health Technology Assessments
Canadian Agency for Drugs and Technologies in Health
International Network of Agencies for Health Technology Assessment
Sources of randomized controlled trials
Central Register of Controlled Trials
Medline (with randomized controlled trial filter)
EMBASE (with randomized controlled trial filter)
Sources of evidence based reviews and evidence summaries
DynaMed
Central Services Agency COMPASS Therapeutic Notes
Sources of national policy
Health Management Information Consortium (HMIC)
Sources of medicines information
The following sources are used by CKS pharmacists and are not necessarily searched by CKS information specialists for all topics. Some of these resources are not freely available and require subscriptions to access content.
British National Formulary (BNF)
electronic Medicines Compendium (eMC)
European Medicines Agency (EMEA)
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