Glaucoma

GlaucomaAnthony King consultant ophthalmic surgeon and honorary associate professor clinicalophthalmology1, Augusto Azuara-Blanco professor of clinical ophthalmology and honorary consultantophthalmologist 2, Anja Tuulonen professor of ophthalmology 3

1NottinghamUniversity Hospital and University of Nottingham, NottinghamNG7 2UH, UK; 2Centre for Vision and Vascular Science, Queens UniversityBelfast, Belfast, UK; 3Tays Eye Centre, Tampere University Hospital, Tampere, Finland

Glaucoma is one of the most common ophthalmic conditionsencountered in primary and secondary care. The World HealthOrganization estimated that in 2010 glaucoma accounted for2% of visual impairment and 8% of global blindness.1Disabilityadjusted life years attributable to glaucoma more than doubledbetween 1990 and 2010 due to the worldwide increase in thenumber of older people.2 Glaucoma is the leading cause ofirreversible blindness in the world. In the United Kingdom, themanagement of patients with glaucoma constitutes a major partof ophthalmologists’ workload, accounting for 23% of allfollow-up attendances to the UK hospital eye service.3 In theNHS there are more than one million glaucoma related visitsper year. The social and economic burden is likely to increasein the future because of longer life expectancy and an ageingpopulation.4 5 In the UK, glaucoma is the second most commoncause for registration of visual impairment, accounting for9-12% of registrations in people over the age of 65 years.6

What is glaucoma?Glaucoma refers to a group of conditions with heterogeneouscauses that results in damage to the optic nerve head and lossof visual field. It is usually associated with an increase inintraocular pressure (IOP) above the normal value—usuallyestimated at 21 mm Hg (mean 15.5, ±2 standard deviations,range 10-21). However, surveys show that 20-52% of patientswith glaucoma have IOPwithin the normal range. Primary openangle glaucoma is the most common type of glaucoma,accounting for over 70% of cases. It is an IOP related opticneuropathy that gives rise to characteristic optic disc changesand visual field loss. In its early stages it affects peripheral visualfield only, but as it advances it results in loss of visual acuityand can cause blindness. Some patients with statistically normalIOP develop the characteristic changes associated with openangle glaucoma and are said to have low tension or normalpressure glaucoma.

Who gets glaucoma?Risk factors for primary open angle glaucoma are increasingage and IOP, black ethnicity, history in a first degree relative,myopia, and diabetes (table 1⇓).4 5 7

A recent meta-analysis showed a substantial variation inprevalence rates in adults according to ethnicity, with rates of2.14 (95% confidence interval 1.72 to 2.65), 4.23 (3.07 to 5.83),and 1.41 (1.00 to 2.00) for white, black, and Asian people,respectively.8

A recent systematic review found an estimated prevalence ofglaucoma in a mainly white population aged over 40 years of2.1% (1.7 to 2.5).5 Around 67% of cases are not currentlydetected in Western countries. In white people, the overallprevalence of glaucoma is 0.3 (0.1 to 0.5) in people aged 40years but increases sharply to 3.3% (2.5 to 4.0) in those aged70 years.Advanced glaucoma at presentation is the main risk factor forblindness. In a recent UK survey, 39% of patients with glaucomapresented with advanced disease in at least one eye.9 Those mostat risk include socially disadvantaged people with no familyhistory of glaucoma, those with high IOP, and those who donot attend an optometrist regularly.9-11

Identifiable gene mutations are implicated but account for onlyabout 5% of cases of adult onset glaucoma.12 Although certaingenetic subtypes are more likely to progress towards severedisease, current knowledge of the inheritance of open angleglaucoma suggests that genetic screening would not detect asubstantial number of the currently undetected cases.

How is glaucoma classified?Glaucoma is classified into two major categories according tothe appearance and obstruction of the drainage pathway at theiridocorneal angle (trabecular meshwork) (fig 1⇓). In open angleglaucoma, despite the normal clinical appearance, the aqueousoutflow is restricted, and in closed angle glaucoma tissuephysically obstructs the angle.

Correspondence to: A King [email protected]

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BMJ 2013;346:f3518 doi: 10.1136/bmj.f3518 (Published 11 June 2013) Page 1 of 9

Clinical Review

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Summary points

The treatment of glaucoma can prevent or slow visual lossA large proportion of people with glaucoma remain undiagnosedPatients with advanced glaucoma at diagnosis are at greatest risk of blindnessThe only treatment strategy with supporting evidence is the lowering of intraocular pressureNon-adherence to glaucoma treatment drops may contribute to disease progression

Sources and selection criteria

This review focuses mainly on the diagnosis and current treatment options for primary open angle glaucoma, which is the most prevalentform in the United Kingdom. We searched Medline, the Cochrane Database of Systemic Reviews, and Clinical Evidence online using thesearch terms “glaucoma”, “glaucoma diagnosis”, “glaucomamedications”, and “glaucoma surgery”. We limited our studies to those conductedin adults and focused on systematic reviews, meta-analyses, and high quality randomised trials when available.

Glaucoma can also be classified according to whether it isprimary (idiopathic; the most common type) orsecondary—associated with detectable comorbidity. Suchcomorbidities include pseudoexfoliation; rubeosis associatedwith ocular ischaemia due to vascular occlusion or diabetes;uveitis; or after ocular surgery, such as retinal detachmentsurgery.The pathophysiology of primary open angle glaucoma is notwell understood. Increased IOP is common and thought to becaused by increased resistance to aqueous outflow at thetrabecular meshwork level. Loss of vision is caused by damageto and death of retinal ganglion cells. The primary site of injuryin glaucoma is thought to be the optic nerve head, where theaxons of the retinal ganglion cells are grouped together.Several factors are thought to cause or contribute to ganglioncell death. Increased pressure may mechanically compress thenerve fibres at the optic nerve head and lamina cribrosa throughwhich they pass. Poor support from the collagenous laminacribrosa causes stasis in axoplasmic flow. Vascular factors suchas perfusion and ischaemia at the optic nerve head may have arole—for example, haemorrhages at the optic nerve head arerelatively common and often predict future progression ofglaucoma (fig 2⇓).Angle closure glaucoma is caused by ocular tissues, usually theiris, mechanically obstructing the drainage pathway andpreventing aqueous outflow through the trabecular network.

What is the natural course of glaucoma?The natural course of open angle glaucoma is variable and timedependent. In many cases glaucoma is preceded by ocularhypertension—raised IOP in the absence of structuralabnormalities of the optic disc or functional abnormality of thevisual field. Ocular hypertension affects 3-5% of the populationover 40 years of age,13 but only a small proportion of thesepeople develop glaucoma.14 15

When glaucoma is manifest characteristic abnormalities can bedetected in the optic nerve head, retinal nerve fibre layer, andvisual field (figs 2 and 3⇓). In most patients with primary openangle glaucoma these abnormalities progress slowly, over years,and patients remain asymptomatic until late in the disease.However progression rates are variable and some types ofsecondary open angle glaucoma often progress more rapidly.Treatment slows down progression, usually through the loweringof IOP.16 17 A systematic review reported that age, dischaemorrhages (for normal tension glaucoma), baseline visualfield loss (severity of disease), baseline IOP, and exfoliationsyndrome (a subtype of open angle glaucoma) were risk factorsfor progression.17

By the time open angle glaucoma becomes symptomatic, severeand irreversible damage has usually occurred to the visual fieldin one or both eyes. In cross sectional population studies indeveloped countries, 3-12% of patients with glaucoma are blindin one or two eyes.7 Some registry based and retrospectivestudies report higher figures—6% blind in both eyes within 15years and 22% within 20 years).7 18

How is the disease identified?The onset of open angle glaucoma is insidious and patients mayhave severe disease despite good visual acuity. Patients withearly glaucoma are typically unaware that they have it, and thosewith more advanced disease may be aware of a shadow in theirvision or a reduction in visual acuity. However, because thevisual fields of both eyes overlap, a normal visual field in oneeye may mask the presence of a defect in the affected eye untilthe disease is fairly advanced. It is difficult to diagnoseglaucoma without facilities to measure IOP and evaluate opticdiscs and visual fields. When glaucoma is suspected, especiallyif recognised risk factors are present (table 1), referral to a localoptometrist or hospital eye service for evaluation is necessary.Some patients with angle closure glaucoma may experience anacute presentation with headache, ocular pain, nausea, vomiting,and blurred vision. Sometimes there are transient symptoms ofblurring of vision and halos around lights, which resolvespontaneously. Patients with angle closure glaucoma are morelikely to be elderly, female, and hypermetropic. More than halfof all patients with glaucoma in the developed world and about90% in developing countries are not identified.5 7 19 Patients arefound through a process of opportunistic case detection, and thewide variation in detection rates is explained by unequal accessto care facilities and large differences in the distribution andquality of services between healthcare systems. The costeffectiveness of systematic screening for glaucoma remainsuncertain.5 20 Screening is not recommended in the UK.Diagnostic evaluation consists of examination of the chamberangle (for example, using gonioscopy), measurement of IOP,fundus examination, and a visual field test.7 21 Measurement ofIOP shows sizeable interobserver and intraobserver variability.21Even if evaluation of IOP was reliable, alone it is insufficientfor diagnosis and screening because it misses 20-52% of patientswith manifest disease.22

Accurate detection of glaucoma is challenging, particularly inearly disease. In the UK a large proportion of patients referredfrom primary care (typically from community optometrists) forglaucoma do not have the disease. Population based studiesshow that 50% of newly detected patients had recently beenseen by an ophthalmologist or optometrist but their disease had



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not been diagnosed.20 Several automated technologies forimaging and measurements for visual function have beendeveloped to aid diagnosis and follow-up of glaucoma (figs 2and 3).

How cost effective is treatment ofglaucoma and ocular hypertension?The treatment of glaucoma has been shown to be clinicallybeneficial and cost effective in preventing disease progressionand visual disability.23 24However, it is unclear whether treatingthose at risk—for example, patients with ocular hypertension—iscost effective.23

Cost effectiveness analyses of interventions typically useefficacy data based on randomised trials, which may provideoptimistic estimates of outcomes compared with “real life,”where adherence to care by patients and clinicians may bepoorer. More reliable and realistic data from pragmaticrandomised trials or cohort studies are therefore needed.23

What are the principles of glaucomamanagement?Management aims to prevent visual disability during a patient’slifetime or, where disability exists, to prevent furtherdeterioration.Currently, the only modifiable risk factor is IOP, the reductionof which minimises the risk of developing glaucoma and ofglaucoma progression. A meta-analysis recently assessed theeffectiveness of IOP lowering treatment to delay thedevelopment of glaucoma in ocular hypertension, as well asprogression of disease in those with open angle glaucoma.24 Itshowed that lowering IOP significantly reduced progression toglaucoma (hazard ratio 0.56, 0.39 to 0.81; P=0.01; numberneeded to treat (NNT) 12). Pooled data of studies in glaucomashowed a significant delay of visual field deterioration (0.65,0.49 to 0.87; P=0.003; NNT=7), with subgroup analysis showinga larger effect in patients with raised IOP.Once a patient is diagnosed with glaucoma a target pressure fortreatment is established. This is an estimate of the IOP believedto be sufficient to prevent disease progressing to a level thatwould impair the quality of life. In general, the younger thepatient and the more severe the glaucoma the lower the targetIOP will be set.7 13 25 There is no universally accepted processfor setting target pressure and several different approaches havebeen suggested.Some patients, particularly older ones with non-severe normalpressure glaucoma, may be monitored and not treated becauseprogression is often slow and may not result in noticeabledisability during their lifetime.For angle closure glaucoma, in addition to lowering IOP, thedrainage pathway needs to be opened. A laser peripheraliridectomy, which punches a hole in the iris, or cataract surgery,which allows the iris to move away from the drainage pathway,is often successful

What are the treatment options forreducing IOP?Medical, laser, and surgical options are available for loweringIOP. Typically, the patient is started on glaucoma dropmonotherapy, with extra drops being added as required, so thattwo or more different types of drug can be used in cases thatare difficult to control. If the maximum tolerated treatment

regimen is unsuccessful, a laser intervention may be advised orthe patient may proceed directly to surgery. The NationalInstitute for Health and Care Excellence and other advisorybodies have developed guidelines to inform treatment pathwaysfor glaucoma.7 13 25

A recent Cochrane review of primarymedical, laser, and surgicalinterventions for glaucoma suggested that a greater reductionin IOP is achieved with primary surgery than with drugs, butthat surgery is associated with more eye discomfort and anincreased requirement for cataract surgery in the short term.26However, the review did not include recent trials that evaluatedcurrently available drugs for glaucoma or modern surgicalmethods.

Medical managementSeveral classes of drops are available (table 2⇓). They lowerIOP by reducing the production or increasing the outflow ofaqueous humour from the eye. Prostaglandin analogues areusually the initial treatment choice because they have thegreatest IOP lowering efficacy and lowest side effect profile. Ifmonotherapy is insufficient to control IOP additional drops areadded. Many drops come as combinations of a β blocker andanother drug. These combinations reduce the numbers of bottlesthat a patient requires and also reduce the preservative loaddelivered to the eye, thus reducing the risk of intolerance orallergy to the preservative used and improving adherence andpersistence. Eyes drops often cause transient stinging andblurring on instillation and somemay cause redness, discomfort,eyelash growth, periorbital skin pigmentation, and an unpleasanttaste. Systemic side effects are rare, although β blockers shouldbe avoided in those with obstructive airways disease or heartfailure.All classes of glaucoma drops are now available as genericpreparations. A variety of guidelines provide algorithms formedical treatment.13 Intolerance to drops (such as chronicdiscomfort, redness of the eye or of the skin around the eye)may be related to the preservative used. In such cases,preservative-free drugs may be used. Treatment with oralcarbonic anhydrase inhibitors (which reduce aqueousproduction) is usually poorly tolerated—patients may experiencetingling in their fingers and toes, lethargy, and loss ofappetite—making it unsuitable for long term treatment but usefulfor controlling acute increases in pressure or managing raisedIOP in the short term while awaiting surgery.Adherence to glaucoma drops is variable and difficult toevaluate.27 It is therefore hard to know whether poor control ofIOP is due to the lack of therapeutic effect or failure of patientsto use the drops. Estimates of non-adherence vary greatlybecause there is no objective method of assessment, makingevaluation of true non-adherence difficult.28Cognitive problemsrelated to understanding the need for drops or forgetfulness,difficulty administering the drops, poor communication betweendoctor and patient, and a lack of engagement by the patient maycontribute to poor adherence. The authors of a recent Cochranereview of interventions for adherence could not recommend anyparticular interventions for improving adherence.29

If IOP is not controlled once the maximum tolerated treatmentregimen is reached (all the drops that a patient can tolerate andacetazolamide in those who can tolerate it), laser or surgicalintervention may be needed.

Laser treatmentLaser trabeculoplasty for open angle glaucoma lowers the IOPby increasing outflow and can be considered as an initial



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treatment option. This is a clinic based procedure. There areseveral laser types. Although laser trabeculoplasty is safe andeffective in lowering IOP, it is not commonly used in the UK.A recent systematic review of laser trabeculoplasty highlightedthe lack of data comparing the effectiveness of this procedurewith modern medical and surgical options.30 Cyclodiode andendocyclodiode laser of the ciliary body are used for severeglaucoma if standard surgery is not effective.

SurgerySurgery is usually undertaken once medical or laser options fortreatment have failed. However, it may be used earlier—forexample, in patients with a disability that prevents them frominstilling drops successfully, those in whom adherence is poor,those presenting with advanced glaucoma,13 and in undevelopedcountries where medical management is not feasible.The standard glaucoma operation (trabeculectomy) creates aguarded fistula into the wall of the eye (sclera), which allows aslow egression of aqueous humour from the anterior chamberinto the subconjunctival space. It is often augmented with anantimetabolite agent to minimise the risk of postoperativescarring, which causes the operation to fail. This operation issuccessful in most patients,31with about 90% of patients havingan IOP of less than 21 mm Hg at 12 months. Failure of surgerywill necessitate re-introduction of drops to control IOP. It is notuncommon for patients who have not already had a cataractoperation to develop cataract and require cataract surgery. Severesight threatening complications, although rare, may also occur.More recently “non-penetrating” glaucoma surgery has becomepopular in some countries—it does not achieve the IOPreduction of trabeculectomy but has a lower adverse eventprofile. However, no large randomised controlled trials havecompared these two interventions.In cases where standard surgery is unsuccessful or for a fewspecific types of glaucoma, glaucoma drainage devices or“tubes” are inserted into the eye; these drain the aqueous humourfrom the anterior chamber into the subconjunctival space.32

How is glaucoma monitored?Once diagnosed, glaucoma requires lifelong monitoring,typically in secondary care. IOP is monitored and functionalvisual change is evaluated through visual field testing.Monitoring structural changes in the optic disc and nerve fibrelayer morphology through photography, scanning lasertechnologies, or optical coherence tomographymay also provideinformation on the stability or progression of the disease (figs2 and 3). The monitoring interval depends on the severity ofglaucoma and the patient’s age. Typically, stable glaucoma willbe monitored every six to 12 months, with advanced glaucomaor progressive glaucoma being monitored every two to fourmonths until stable. It can be difficult to detect small amountsof visual field progression, however, because of the inherentvariability in visual field testing, and several visits may beneeded to establish progression.

Are there any restrictions to driving withglaucoma?Glaucoma can impair driving ability,33 34 and patients may havean increased risk of motor vehicle crashes.35 36 Retention ofdriving ability is highly important to these patients.37 In the UK,visual field and visual acuity criteria are used to define eligibilityto drive. Although most patients are able to drive, patientsdiagnosed with glaucoma are obliged to report the diagnosis to

the Driver and Vehicle Licensing Agency. Severe loss ofbinocular visual field may affect eligibility to drive.

What future treatments are on thehorizon?Improvement in drug delivery systems to allow sustained slowrelease of drugs as drops or through an intraocular implant mayimprove adherence, improve the efficacy of these drugs toreduce IOP, and reduce ocular surface symptoms associatedwith the use of glaucoma drops.Development of a therapeutic intervention that providesneuroprotection for the retinal ganglion cells that undergoapoptosis may help prevent further visual loss. To date, no drugshave shown clinical evidence of a neuroprotective effect inglaucoma.38

Stem cells and gene transfer could potentially improve trabecularmeshwork outflow and reduce the IOP. There is also interest ininvestigating the potential role of stem cell transplantation forretinal ganglion cell regeneration.

Thanks to Antti Pollari, Tays Eye Centre, for the retinal nerve fibre layerimages featured in fig 1.Contributors: All authors helped with the idea for and design of themanuscript, drafting the article or revising it critically for importantintellectual content, and final approval of the version to be published.AK is guarantor.Competing interests: We have read and understood the BMJ Grouppolicy on declaration of interests and declare the following interests:None.Provenance and peer review: Commissioned; externally peer reviewed.

1 WHO. Global data on visual impairments 2010. www.who.int/blindness/GLOBALDATAFINALforweb.pdf.

2 Murray CJ, Vos T, Lozano R, Naghavi M, Flaxman AD, Michaud C, et al. Disability-adjustedlife years (DALYs) for 291 diseases and injuries in 21 regions, 1990-2010: a systematicanalysis for the Global Burden of Disease Study 2010. Lancet 2012;380:2197-223.

3 Spry PG, Spencer IC, Sparrow JM, Peters TJ, Brookes ST, Gray S, et al. The BristolShared Care Glaucoma Study: reliability of community optometric and hospital eye servicetest measures. Br J Ophthalmol 1999;83:707-12.

4 Coleman AL, Miglior S. Risk factors for glaucoma onset and progression. Surv Ophthalmol2008;53(suppl 1):S3-10.

5 Burr JM, Mowatt G, Hernandez R, Siddiqui MA, Cook J, Lourenco T, et al. The clinicaleffectiveness and cost-effectiveness of screening for open angle glaucoma: a systematicreview and economic evaluation. Health Technol Assess 2007;11:iii-iv, ix-x, 1-190.

6 Bunce C, Xing W, Wormald R. Causes of blind and partial sight certifications in Englandand Wales: April 2007-March 2008. Eye (Lond) 2010;24:1692-9.

7 Tuulonen A, Airaksinen PJ, Erola E, Forsman E, Friberg K, Kaila M, et al. The Finnishevidence-based guideline for open-angle glaucoma.Acta Ophthalmol Scand 2003;81:3-18.

8 Rudnicka AR, Mt-Isa S, Owen CG, Cook DG, Ashby D. Variations in primary open-angleglaucoma prevalence by age, gender, and race: a Bayesian meta-analysis. InvestOphthalmol Vis Sci 2006;47:4254-61.

9 Ng WS, Agarwal PK, Sidiki S, McKay L, Townend J, Azuara-Blanco A. The effect ofsocio-economic deprivation on severity of glaucoma at presentation. Br J Ophthalmol2010;94:85-7.

10 Fraser S, Bunce C, Wormald R. Risk factors for late presentation in chronic glaucoma.Invest Ophthalmol Vis Sci 1999;40:2251-7.

11 Sukumar S, Spencer F, Fenerty C, Harper R, Henson D. The influence of socioeconomicand clinical factors upon the presenting visual field status of patients with glaucoma. Eye(Lond) 2009;23:1038-44.

12 Fingert JH. Primary open-angle glaucoma genes. Eye (Lond) 2011;25:587-95.13 National Institute for Health and Clinical ExcellenceGlaucoma. Diagnosis andmanagement

of chronic open angle glaucoma and ocular hypertension. CG85. 2009. www.nice.org.uk/nicemedia/live/12145/43839/43839.pdf.

14 Kass MA, Heuer DK, Higginbotham EJ, Johnson CA, Keltner JL, Miller JP, et al. TheOcular Hypertension Treatment Study: a randomized trial determines that topical ocularhypotensive medication delays or prevents the onset of primary open-angle glaucoma.Arch Ophthalmol 2002;120:701-13; discussion 829-30.

15 Miglior S, Zeyen T, Pfeiffer N, Cunha-Vaz J, Torri V, Adamsons I. Results of the EuropeanGlaucoma Prevention Study. Ophthalmology 2005;112:366-75.

16 Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control ofintraocular pressure and visual field deterioration. AGIS Investigators. Am J Ophthalmol2000;130:429-40.

17 Ernest PJ, Schouten JS, Beckers HJ, Hendrikse F, Prins MH, Webers CA. Anevidence-based review of prognostic factors for glaucomatous visual field progression.Ophthalmology 2012; published online 1 Dec.

18 Hattenhauer MG, Johnson DH, Ing HH, Herman DC, Hodge DO, Yawn BP, et al. Theprobability of blindness from open-angle glaucoma. Ophthalmology 1998;105:2099-104.



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http://www.who.int/blindness/GLOBALDATAFINALforweb.pdf

http://www.who.int/blindness/GLOBALDATAFINALforweb.pdf

http://www.nice.org.uk/nicemedia/live/12145/43839/43839.pdf

http://www.nice.org.uk/nicemedia/live/12145/43839/43839.pdf



Questions for future research

Should laser trabeculoplasty be used as primary treatment for mild and moderate glaucoma?What is the most cost effective way of monitoring and managing ocular hypertension and manifest glaucoma?What role do other healthcare professionals (such as optometrists and ophthalmic technicians) and technology have in improving theefficiency of monitoring of glaucoma?Can we monitor glaucoma in the community?What is the most effective and cost effective way to prevent blindness for those presenting with advanced glaucoma?

Future research

Evaluation of technologies for diagnosing and monitoring glaucomaEvaluation of new drug delivery systems to ensure 24 hour control of intraocular pressure and minimise the risks of poor control associatedwith non-adherenceDevelopment of safer and more effective surgical techniquesEvaluations of the most cost effective models of care for treating and monitoring ocular hypertension and primary open angle glaucomaEvaluation of the most cost effective interventions for those presenting with advanced glaucomaThe role of neuroprotection and neuroregeneration in the treatment of glaucoma

Additional educational resources

Resources for healthcare professionalsRoyal College of Ophthalmologist (www.rcophth.ac.uk/page.asp?section=484&sectionTitle=Current±Issues±in±Glaucoma)—Currentissues in glaucomaThe following four websites provide information about the symptoms, diagnosis, and treatment of glaucomaEuropean Glaucoma Society (http://www.eugs.org/eng/default.asp)American Academy of Ophthalmology (http://one.aao.org/ce/default.aspx)World Glaucoma Association (http://www.worldglaucoma.org/)College of Optometrists (www.college-optometrists.org)

Resources for patientsInternational Glaucoma Association (www.glaucoma-association.com/)—Comprehensive source of up-to-date news and informationabout glaucomaRoyal College of Ophthalmologists (www.rcophth.ac.uk/page.asp?section=365&sectionTitle=Information+Booklets)—Information bookletsAmerican Academy of Ophthalmology (www.geteyesmart.org/eyesmart/diseases/glaucoma.cfm)—Information about the causes,symptoms, diagnosis and treatment of glaucomaEuropean Glaucoma Society (http://www.eugs.org/eng-paz/default.asp )—Information on ocular pressure and glaucomaCollege of Optometrists (www.college-optometrists.org/en/knowledge-centre/publication/patient-leaflets/index.cfm)—Patient leaflets onglaucoma

19 Wittenborn JS, Rein DB. Cost-effectiveness of glaucoma interventions in Barbados andGhana. Optom Vis Sci 2011;88:155-63.

20 Vaahtoranta-Lehtonen H, Tuulonen A, Aronen P, Sintonen H, Suoranta L, Kovanen N,et al. Cost effectiveness and cost utility of an organized screening programme forglaucoma. Acta Ophthalmol Scand 2007;85:508-18.

21 Burr JM, Botello-Pinzon P, Takwoingi Y, Hernandez R, Vazquez-Montes M, Elders A, etal. Surveillance for ocular hypertension: an evidence synthesis and economic evaluation.Health Technol Assess 2012;16:1-271, iii-iv.

22 Heijl A, Leske MC, Bengtsson B, Hyman L, Hussein M. Reduction of intraocular pressureand glaucoma progression: results from the Early Manifest Glaucoma Trial. ArchOphthalmol 2002;120:1268-79.

23 Tuulonen A. Cost-effectiveness of screening for open angle glaucoma in developedcountries. Indian J Ophthalmol 2011;59(suppl):S24-30.

24 Maier PC, Funk J, Schwarzer G, Antes G, Falck-Ytter YT. Treatment of ocular hypertensionand open angle glaucoma: meta-analysis of randomised controlled trials. BMJ2005;331:134.

25 Heijl A, Alm A, Bengtsson B, Bergstrom A, Calissendorff B, Lindblom B, et al. Theglaucoma guidelines of the Swedish Ophthalmological Society. Acta Ophthalmol Suppl(Oxf) 2012;251:1-40.

26 Burr J, Azuara-Blanco A, Avenell A, Tuulonen A. Medical versus surgical interventionsfor open angle glaucoma. Cochrane Database Syst Rev 2012;9:CD004399.

27 Kass MA, Gordon M, Meltzer DW. Can ophthalmologists correctly identify patientsdefaulting from pilocarpine therapy? Am J Ophthalmol 1986;101:524-30.

28 Olthoff CM, Schouten JS, van de Borne BW, Webers CA. Noncompliance with ocularhypotensive treatment in patients with glaucoma or ocular hypertension an evidence-basedreview. Ophthalmology 2005;112:953-61.

29 Gray TA, Orton LC, Henson D, Harper R, Waterman H. Interventions for improvingadherence to ocular hypotensive therapy.Cochrane Database Syst Rev 2009;2:CD006132.

30 Rolim de Moura C, Paranhos A Jr, Wormald R. Laser trabeculoplasty for open angleglaucoma. Cochrane Database Syst Rev 2007;4:CD003919.

31 Wong MH, Husain R, Ang BC, Gazzard G, Foster PJ, Htoon HM, et al. The Singapore5-Fluorouracil Trial: intraocular pressure outcomes at 8 years. Ophthalmology 2013;published online 1 Mar.

32 Gedde SJ, Singh K, Schiffman JC, Feuer WJ. The Tube Versus Trabeculectomy Study:interpretation of results and application to clinical practice. Curr Opin Ophthalmol2012;23:118-26.

33 Haymes SA, LeBlanc RP, Nicolela MT, Chiasson LA, Chauhan BC. Glaucoma and on-roaddriving performance. Invest Ophthalmol Vis Sci 2008;49:3035-41.

34 Szlyk JP, Mahler CL, SeipleW, Edward DP,Wilensky JT. Driving performance of glaucomapatients correlates with peripheral visual field loss. J Glaucoma 2005;14:145-50.

35 Haymes SA, Leblanc RP, Nicolela MT, Chiasson LA, Chauhan BC. Risk of falls andmotorvehicle collisions in glaucoma. Invest Ophthalmol Vis Sci 2007;48:1149-55.

36 Tanabe S, Yuki K, Ozeki N, Shiba D, Abe T, Kouyama K, et al. The association betweenprimary open-angle glaucoma and motor vehicle collisions. Invest Ophthalmol Vis Sci2011;52:4177-81.

37 Bhargava JS, Patel B, Foss AJ, Avery AJ, King AJ. Views of glaucoma patients on aspectsof their treatment: an assessment of patient preference by conjoint analysis. InvestOphthalmol Vis Sci 2006;47:2885-8.

38 Sena DF, Lindsley K. Neuroprotection for treatment of glaucoma in adults. CochraneDatabase Syst Rev 2013;2:CD006539.

Cite this as: BMJ 2013;346:f3518© BMJ Publishing Group Ltd 2013



CLINICAL REVIEW

http://www.rcophth.ac.uk/page.asp?section=484&sectionTitle=Current�Issues�in�Glaucoma

http://www.eugs.org/eng/default.asp

http://one.aao.org/ce/default.aspx

http://www.worldglaucoma.org/

http://www.college-optometrists.org/

http://www.glaucoma-association.com/

http://www.rcophth.ac.uk/page.asp?section=365&sectionTitle=Information+Booklets

http://www.geteyesmart.org/eyesmart/diseases/glaucoma.cfm

http://www.eugs.org/eng-paz/default.asp

http://www.college-optometrists.org/en/knowledge-centre/publication/patient-leaflets/index.cfm



Tables

Table 1 | Risk factors for glaucoma5

Pooled adjusted relative risk (95% CI)Pooled % prevalence (95% CI)Risk factor

3.8 (2.6 to 5.6)Not availableBlack ethnicity

12.6 (5.1 to 31.2)Not availableIntraocular pressure >26 mm Hg

1.9 (1.5 to 2.3)2.7 (1.5 to 3.9)Myopia

2.1 (1.4 to 3.0)3.3 (1.8 to 4.8)Diabetes

3.1 (2.3 to 4.5)6.7 (5.0 to 8.4)Family history



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Table 2| Eye drops for treating glaucoma: class and mechanism of action

DrugDaily dosesMechanismClass

Latanoprost*†1Increase outflowProstaglandin analogues

Travoprost

Bimatoprost*

Tafluprost*

Timolol*†1 or 2Decrease aqueous productionβ blockers

Betaxolol*†

Levobunolol*

Carteolol

Apraclonidine*2 or 3Increase outflow; decrease aqueous productionα agonists

Brimonidine†

Dorzolamide*†2 or 3Decrease aqueous productionCarbonic anhydrase inhibitors

Brinzolamide†

Pilocarpine*†4Increases outflowParasympathomimetic

*Preservative-free preparations available; †generic preparations available.



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Figures

Fig 1 Classification of glaucoma by mechanism and appearance of the anterior chamber angle. Patients with primary andsecondary closed angle glaucoma can present with acute attacks. These are characterised by very high intraocular pressureand symptoms such as headache, nausea, vomiting, and blurred vision

Fig 2 The top panel shows the development (over 12 months) of a nerve fibre layer defect (darker wedge between whitearrows) in a patient with early glaucoma emanating from the edge of the optic disc. The bottom panel (left eye of the samepatient) shows a disc margin haemorrhage (black arrow) with associated nerve fibre layer defect (wedge between red-brownarrows), which widens over the next 12 months



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Fig 3 Example of glaucomatous disc with disc cupping and an associated early visual field defect. Imaging of the sameoptic disc topography is shown using Heidelberg retinal tomography on the left and peripapillary nerve fibre layer thicknessevaluation with ocular coherence topography on the right



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