apg guidelines nm view

8/12/2019 Apg Guidelines Nm View

http://slidepdf.com/reader/full/apg-guidelines-nm-view 1/103

www.seag ig .org

A S I A P A C I F I CGlaucoma Guidelines

With the support of the Asian-Oceanic Glaucoma Society



Copyright © 2003–2004 SEAGIG, Sydney.

All rights reserved. No part of this publication may be reproduced, stored in a retrievalsystem or transmitted in any form or any means – electronic, mechanical, photocopying,recording or otherwise – without the prior permission of SEAGIG.

DISCLAIMER

These guidelines for clinical practice are based on the best available evidence at thetime of development. They are not intended to serve as standards of medical care.The use of these recommendations is the decision of each clinician, who is ultimatelyresponsible for the management of his/her patient. The South East Asia GlaucomaInterest Group (SEAGIG) and the Asian-Oceanic Glaucoma Society (AOGS), together withthe contributors, reviewers, sponsor and publisher, disclaim responsibility and liabilityfor any injury, adverse medical or legal effects resulting directly or indirectly from theuse of these Guidelines. All clinical diagnoses, procedures and drug regimens/doses mustbe independently verified. All products mentioned in this publication should be used inaccordance with the manufacturers’ instructions or prescribing information.

ISBN 0-9751692-0-3

Printed in Singapore



A S I A P A C IGlaucoma Guide



Foreword

By increasing awareness and knowledge of glaucoma aPacific region, these Guidelines aim to reduce glaucomdisability and to provide a rational basis for glaucoma

The establishment of best-practice methodologies thro

Pacific region represents a unique challenge, given ourservice systems and wide range of available resources. need, the South East Asia Glaucoma Interest Group (SEsupport of the Asian-Oceanic Glaucoma Society (AOGS)Asia Pacific Glaucoma Guidelines Working Party to devGlaucoma Guidelines for the Asia Pacific region.

The members of the Working Party collaborated duringmeetings to compile information and recommendationcomprehensive ophthalmologists, general healthcare aprofessionals, as well as healthcare policy makers to deglaucoma management to their communities. An extenCommittee assessed the results and made significant cothe final manuscript.

As these Guidelines rely on direct medical experience apossible, on published evidence, they are as up-to-dateThe Asia Pacific Glaucoma Guidelines Working Party is providing updates to the Guidelines on a regular basis.

Critical to the development of the Asia Pacific Glaucombeen the support of the AOGS, and a generous educatthen Pharmacia Corporation (now Pfizer Inc.). This sponthe Working Party to meet and to produce, publish andGuidelines.



Members of the Working Party

Haruki Abe (Japan)

Manuel Agulto (Philippines)

Paul Chew (Singapore)

Paul Foster (UK)

Ivan Goldberg (Australia), Chair

Paul Healey (Australia)

Prin RojanaPongpun (Thailand)

Hidenobu Tanihara (Japan)

Ravi Thomas (India)

Ningli Wang (China)

Contributors

Gus Guzzard (UK)

Ching Lin Ho (Singapore)



Ropilah Abdul Rahman (Malaysia)

Edi Affandi (Indonesia)

Harish Agarwal (India)

P Juhani Airaksinen (Finland)

Mario V Aquino (Philippines)

Makoto Araie (Japan)

Gomathy Arumugam (Malaysia)

Stephen Best (New Zealand)

Anne MV Brooks (Australia)

G Chandra Sekhar (India)

Guy D’Mellow (Australia)

Ataya Euswas (Thailand)

Seng Kheong Fang (Malaysia)

Adrian Farinelli (Australia)

Stuart Graham (Australia)

John Grigg (Australia)

Amod Gupta (India)

Ralph A Higgins (Australia)

Roger A Hitchings (UK)

Young J Hong (Korea)

Siu Ping Hui (Hong Kong)Por T Hung (Taiwan)

Changwon Kee (Korea)

Patricia M Khu (Philippines)

Don Minckler (U

Anthony CB Mo

William Morgan

Vinay Nangia (In

Stephen A Obstb

Francis Oen (Sing

Julian Rait (Aust

Rengappa Rama

Robert Ritch (US

Ngamkae Ruang

Julian Sack (Aust

Steve Seah (Sing

Ramanjit Sihota

Ikke Sumantri (In

Hem K Tewari (I

John Thygesen (

Aung Tin (Singa

Wasee Tulwatan

Anja Tuulonen (

Lingam Vijaya (I

Prateep Vyas (InTsing-Hong Wan

Robert N Weinre

Hon Tym Wong

Members of the Review Committee



ACKNOWLEDGEMENT

This work was made possible by an unrestricted educationPfizer Inc.

The Asia Pacific Glaucoma Guidelines Working Party wouldespecially for their support:

Bruno ArcoMargarita JimenezAnders Lundqvist

Ian Saunders

MediTech Media Asia Pacific (Project Manager

Hooi Ping CheeM Paguio



Contents

Foreword

Acknowledgement

Introduction

Epidemiology of Glaucoma in Asia

Section 1

1.1 Patient Assessment

1.2 Treatment Categories and Targets

Section 2

2.1 Initiation of Treatment

2.2 Medical Treatment

2.3 Laser Treatment

2.4 Surgery

Section 3

3.1 Follow-up



List of Appendices

Appendix

1 How to test calibration of a Goldmann t

2 Tonometry mires

3a Gonioscopy

3b Goniogram/gonioscopic chart

3c Corneal wedge diagram

4 How to optimize patient

performance in subjective perimetry

5 Secondary glaucomas – principles of man

6 Angle closure mechanisms

7a Argon laser trabeculoplasty

7b Contact transscleral diode laser

8 Glaucomatous optic neuropathy

9 Field progression print-outs



Introduction

In 1996, with the support of the American Glaucoma SoAcademy of Ophthalmology produced its Preferred PraPrimary Open-Angle Glaucoma,1 followed four years latand two additional volumes on Primary Angle Closure3

Angle Glaucoma Suspect.4 These guidelines identify cha

components of quality eye care “commensurate with prand resources” – this translates into guidance for state-of practice, which should be helpful in the care of mostthan any particular individual. Where data permits, thefirmly evidence-based; otherwise they rely on consensusthe European Glaucoma Society published its Terminolofor Glaucoma in 1998,5 with the aim of “improving the

understanding of this disease in addition to providing ato the diagnosis and management of glaucoma”. This yehas been released.6 These projects have set out to compscientific literature, and involved input from many glauThe resulting publications have proven useful for, and tcomprehensive ophthalmologists around the world. Theuseful in communications with allied eye healthcare pro

as governmental agencies and non-governmental organ

Over the past 20 years, increasing epidemiological data Asia Pacific region has highlighted the varying prevalenrates, diagnostic types and behavior of different glaucoencountered by the ophthalmological community. Withthis information, the need for similar guidelines relevannow be met. Such guidelines must be sensitive to the w

human, structural and equipment resources available thregion, as well as the ethnic diversity of our communitiapplicable in one country or location may not be in ano

These Guidelines have been developed during a time of



In the development of these Guidelines, we have tried t

evidence, and to stratify the recommendations accordinThis has allowed us to clarify and to append to these Guareas for further research. It is hoped this will facilitate omutually supportive ophthalmic community.

How widespread is the problem? What are the risk factodiffer from elsewhere? The section on Epidemiology trie

questions. How do we take a focused history, perform aexamination? What additional tests might we consider feither in the presence or absence of glaucoma? What is developing glaucoma? What is the degree of damage ifalready present? What is the risk of glaucoma progressinAssessment tackles these, both for initiation of therapy

The Treatment Categories and Targets section helps us tindividual patient, therapeutic goals to severity of glaucglaucoma has been divided into medical, laser and surgidetection is considered from both population screening points of view.

These guidelines have been developed in an easy-to-reabenefit of comprehensive ophthalmologists, other eye c

our healthcare colleagues. The format answers question‘when?’, ‘how?’ and ‘for whom?’. We strongly recommeexamines the entire Guidelines before applying informasection to the care of an individual patient.

As with all treatment guidelines, this publication is not aautomated care. By adapting the guidelines with respec

individual needs, the socio-economic environment and mavailable, as well as your own experience, we hope the excellent care will be achieved.

Ivan Goldberg



References

1 American Academy of Ophthalmology. Preferred Practice PatterGlaucoma, 1996.

2 American Academy of Ophthalmology. Preferred Practice PatterGlaucoma, 2000.

3 American Academy of Ophthalmology. Preferred Practice PatteClosure, 2000.

4 American Academy of Ophthalmology. Preferred Practice PatterGlaucoma Suspect , 2000.

5 European Glaucoma Society. Terminology and Guidelines for GlDogma.

6 European Glaucoma Society. Terminology and Guidelines for Gl2003, Italy: Dogma.



Asia Pacific Glaucoma Guidelines



Epidemio

Epidemiology of Glaucoma in Asia

Glaucomatous optic neuropathy (GON) is most prevaleAfrican origin, and least prevalent in full-blooded AustAsian populations have rates intermediate between thEuropean- and African-derived peoples suffer predomiopen angle glaucoma (POAG), whereas rates of primar

glaucoma (PACG) are higher among East Asians than inAlthough a direct and exact comparison of POAG rateslikely has a similar prevalence in Asian and European phigher rate of GON in those of Chinese extraction is prto the excess of PACG.2 Rates on the Indian subcontinebetween studies, although these differences are probaIn absolute terms, there are large numbers of people s

and POAG in India. Preliminary data suggests that prevless in Southeast Asian populations than in the ChineseEuropeans.

Incidence rates of symptomatic acute angle closure (givpersons/year for the population aged 30 years and oveEurope (Finland)3 to 15.5 in Chinese Singaporeans.4 Mapeople in Singapore have lower rates than Chinese Sin6.3, respectively).5

Population surveys in Mongolia found glaucoma to be of blindness in adults (cataract being the cause of 36%Among Chinese Singaporeans, 60% of adult blindness glaucoma.7 Cautious extrapolation of these data sugge1.7 million people in China suffer blindness caused by g

responsible for the vast majority (91%) of these cases.2

glaucoma is the most common cause of uniocular blind

Glaucoma is the leading cause of registered, permanenHong Kong (23%).8 In Japan, diabetic retinopathy (18%

Incidence of symptomatic,‘acute’ angleclosure

Glaucomablindness




Although angle closure is associated with a hyperme

cases do occur in myopes. A shallow anterior chamberecognized to be a factor that predisposes toward andepth of the anterior chamber reduces with age andin women than in men.21,22 There may also be an assomyopia and POAG.23 In India, pseudoexfoliation was cases of POAG.24

References:

1. Royal Australian and New Zealand College of OphthalmoloTrachoma and Eye Health Program, Chapter 8, pp. 82–100,

2. Foster PJ, Johnson GJ. Glaucoma in China: how big is the p2001;85:1277–1282.

3. Teikari J, Raivio I, Nurminen M. Incidence of acute glaucom1982. Graefe's Arch Clin Exp Ophthalmol 1987;225:357–360

4. Seah SKL, Foster PJ, Chew PT, et al . Incidence of acute primglaucoma in Singapore. An Island-Wide Survey. Arch Ophth1997;115:1436–1440.

5. Wong TY, Foster PJ, Seah SKL, et al . Rates of hospital admisclosure glaucoma among Chinese, Malays, and Indians in Si2000;84:990–992.

6. Baasanhu J, Johnson GJ, Burendei G, et al . Prevalence and cvisual impairment in Mongolia: a survey of populations ageWorld Health Organization 1994;72:771–776.

7. Foster PJ, Oen FT, Machin DS, et al . The prevalence of glauc

of Singapore. A cross-sectional population survey in TanjonOphthalmol 2000;118:1105–1111.

8. Hong Kong Hospital Authority Statistical Report 2001–2002permanent blindness in hospital authority ophthalmology thttp://www.ha.org.hk (accessed 27 Sept 2003).

9 Tso MOM Naumann GO Zhang S Editorial Studies of the



Epidemio

14. Wensor MD, McCarty CA, Stanislavsky YL, et al . The prevalenc

Melbourne Visual Impariment Project. Ophthalmology 1998;115. Mitchell P, Smith W, Attebo W, et al . Prevalence of open-angl

The Blue Mountains Eye Study. Ophthalmology 1996;103:1661

16. Shiose Y, Kitazawa Y, Tsukuhara S, et al . Epidemiology of glaunationwide glaucoma survey. Jpn J Ophthalmol 1991;35:133–1

17. Leske MC, Connell AM, Wu SY, et al . Risk factors for open angBarbados Eye Study. Arch Ophthalmol 1995;113(7):918–24.

18. McNaught AI, Allen JG, Healey DL, et al . Accuracy and implicafamily history of glaucoma: experience from the Glaucoma InTasmania. Arch Ophthalmol 2000;118(7):900–904.

19. Foster PJ, Machin D, Wong TY, et al . Determinants of intraocuassociation with glaucomatous optic neuropathy in Chinese STanjong Pagar Study. Invest Ophthalmol Vis Sci 2003;44(9):388

20. Törnquist R. Shallow anterior chamber in acute angle-closurestudy. Acta Ophthalmol 1953;31(Suppl. 39):1–74.

21. Okabe I, Taniguchi T, Yamamtoo T, et al .. Age-related changechamber width. J Glaucoma 1992;1:100–107.

22. Foster PJ, Alsbirk PH, Baasanhu J, et al . Anterior chamber depVariation with age, sex and method of measurement. Am J O1997;124:53–60.

23. Mitchell P, Hourihan F, Sandbach J, et al . The relationship betwmyopia. The Blue Mountains Eye Study. Ophthalmology 1999;

24. Krishnadas R, Nirmalan PK, Ramakrishnan R, et al . Pseudoexfopopulation of southern India: the Aravind Comprehensive EyeOphthalmol 2003;135:830–7.



Section 1



1.1 Patient Assessment

The purpose of this section is to describe the initial assein whom glaucoma is suspected, from the perspective othe developed and developing worlds. Inevitably, somemore relevance to one or other setting, however, time a patient is seldom wasted. The initial consultation lays

for successful management of the patient.

Assessment of a child with suspected glaucoma raises squestions. Such a child should be referred urgently to a

The aims during the initial assessment are:

• to determine whether or not glaucoma is present, o(i.e., assess risk factors)

• to exclude or confirm alternative diagnosis

• to identify the underlying mechanism of damage, sochoice of management

• to begin planning a strategy of management

• to identify suitable forms of treatment, and to excluinappropriate.

Understand the natural history of the glaucomas in youassessment can be divided into two phases:

1. History

2. Examination/investigations

Key points:

• Most glaucomas, including angle closure glaucoma (asymptomatic until advanced

Why assess?

What toassess?

History

A i P ifi Gl G id li



Past medical history

Consider:Factors that will affect life expectancy and compliancExclude past hemodynamic crises (postpartum hemorabdominal aneurysm, severe trauma) that may causecupping that mimics glaucoma but is not progressive

Specific predisposing diseases are summarized in Tab

Table 1.1: Factors to consider when taking a medicalwith suspected glaucoma


Visual symptoms of glaucoma• Visual blurring and discomfort:

– This may be due to angle closure, Posner-Schlosyndrome or pigment dispersion

• Glare and colored rings around lights from corne– This needs to be differentiated from migraine

• Poor light/dark adaptation

• Difficulty tracking fast-moving objects (e.g., golf

Respiratory Asthma and other chronic obstruc

diseases associated with hyperresand/or reduced lung capacity willtopical β-blockers

Cardiovascular • Cardiac arrhythmias, e.g., heart the use of topical β blockers or



Endocrine • Diabetes – increasingly prevalentwith open angle and neovascular

• Thyroid eye disease

• Pituitary tumors

Central • Previous cerebrovascular accidentnervous system injury/pituitary lesions (field loss)

• Early dementia – affects complianand insight into the disease

Musculo- Arthritis (osteo-, rheumatoid) maskeletal the ability to administer eye drop

Urogenital Urinary stones may limit systemicanhydrase inhibitors (CAIs)

Ocular trauma Angle recession, lens dislocation, damage

Pregnancy and Present or possible, renders all inlactation potentially hazardous

Medication

Use of any current medication needs to be considerecertain specific past medications, including:





Social history

Consider:

• How regularly can the patient attend?

• Can the patient afford and comply with treatment?

• How will having glaucoma affect the patient’s life/wand treatment)?

Family history

Consider:

What is the disease type and course in the family? (S

Examination requires appropriate equipment, sufficieexamination techniques and accurate and reliable re

While resources vary widely across our region, there acceptable standard of equipment and training.

Minimal acceptable resources for examination

• A slit lamp with indirect lens between 60–90D an

ophthalmoscope

• An automated perimeter

• A gonioscope that allows indentation gonioscop

• A Goldmann-style applanation tonometer (or ToMaklakov tonometers are not generally accepta

When the patient cannot get to a slit lamp

• Portable hand held slit lamp may be very useful

• In the absence of a portable slit lamp a jeweler’

Examination/ Investigations



How to perform

Goldmanntonometry?

Intraocular pressure (IOP) is the only modifiable risk fac

Goldmann-style Applanation Tonometry (GAT). (Tonopenot available).

Every visit.

• Ensure tonometer is calibrated (see Appendix 1: Howof a Goldmann tonometer ).

• The prism tip must be disinfected and then disinfect

• The eyelashes must be kept out of the way (avoid pr

• The cornea must be anesthetized.

• The tip must touch the central cornea gently with th

through the slit lamp eyepiece just prior to the tip m(tip: look for the white split ring that will fluoresce wtouches the cornea).

• Adjust the gauge until the split tear meniscus just to

Factors associated with IOP

Table 1.2: Factors affecting measured IOP

Circadian cycle The IOP follows a circadian cycle, ofthe morning and a trough in the evdiurnal variation is 3–6 mmHg

Central corneal Thicker corneas are associated with

thickness IOP measurements, thinner corneas depressed IOP measurements: apply1–3 mmHg/40µ deviation from 525µ

Blood pressure IOP is positively associated with systti l l t li

When?

How to performGoldmanntonometry?

Why?

What?

Slit lampexamination

– tonometry





Table 1.3: Measurement errors associated with GAT 8

IOP reading artificially low • Insufficient fluo

IOP reading artificially high • Excessive fluore

• Eyelid pressure blepharospasm

• Digital pressurelids apart

• Obese patient

• Patient straininchin/forehead r

• Patient breath-

• Patient wearingaround neck (ecollar +/- tie for

• Hair lying acrosdistorting mires

• Lens-corneal ap

Technical difficulties (interpret • Corneal abnormresults with caution) graft, edema)

• Marked cornea

• Small palpebral

N t



Anterior chamber:

• pigment on corneal endothelium (pigment dispersio

• peripheral anterior chamber depth (van Herick techn

• central anterior chamber depth

• evidence of inflammation (e.g., keratic precipitates).

Iris:

• mid-dilated poorly reactive (post angle closure attac

• isolated zones of patch atrophy or spiraling

• rubeosis

• synechiae

• configuration in relation to lens– pseudoexfoliation material on pupil edge– pigment deposit on anterior surface– transillumination defect.

Lens:

• pseudoexfoliation material

• lens thickness and opacity

• phacodonesis

• glaukomflecken.

(See Appendix 3a: Gonioscopy )

Detect angle closure, occludable and secondary glauco

Angle width and characteristics (see below).

• Initially for all.

• Regularly for angle closure patients

Why?

What to look for?

When?

Gonioscopy




• Place lens gently on eye while looking through slit

doing tonometry) – no gel needed with Zeiss-type • Look through the upper mirror (inferior angle) as

stop pushing when you can see the iris.

• Move slit lamp beam inferiorly (avoid pupil) to exa

• Then turn beam 90 degrees and move on axis.

• Move to nasal side (temporal angle) then to temp

• Record findings on goniogram.(see Appendix 3b: Goniogram/Gonioscopic chart )

Tip: If you cannot find the angle structures, use a bright wide slat low magnification. Once you have found the angle structuredown, shorten and narrow the slit and look for the change in irYou may need to wait a minute or so.

Figure 1.4: Gonioscopy flow diagram

Scleral spur visible?

YES

Grade: Record findings

NO

Do indentation gonioscopyAny synechiae?

YES

Grade: Record findingsN

IOP r

YESGrade: Record findings

Open angle

PAC (synechiae)

PAC (apposition)



Defines glaucoma.

• Disc size.

• Neuroretinal rim.

• Disc hemorrhage.

• Nerve fiber layer defect.

• Peripapillary atrophy (PPA).

• Vascular pattern.

Every visit.

Consider:

Non-glaucomatous optic neuropathies. Differentiate anoptic neuropathy (AION) from glaucoma – especially giBoth cause pale cupped disc and field loss.

• Slit lamp.

• Very thin, bright beam for disc measurement.

• Dimmer beam for clearer/artificial lenses.

• Indirect slit lamp lens (60–90D).

• Stereoscopic view (best when dilated – recommende

• Red-free (green) illumination may help assessment o

• Direct ophthalmoscopy or slit lamp view through unlens if pupil small and not able to be dilated.

Figure 1.5: Disc examination flowchart

Why?

What to look

for?

When?

How to perform disc examination?

Optic nerve

head and retinal nerve fiber layer




Table 1.6: Normal vertical cup–disc ratios for vertical

Disc diameter Mean cup–disc ratio≤1.0 0.261.2 0.331.4 0.391.6 0.451.8 0.50≥2.0 0.55

Disc recording

• Draw optic disc (large), rim, key vessels that definesigns.

• Draw notches, shelving, loss to rim–clock hours.

• Record whether nerve fiber layer is visible and assedefects.

• Record vertical cup–disc ratio in the narrowest parrecording the rim–disc ratio at key parts of the rim

• Record disc hemorrhages, baring of circumlinear bvessels bayoneting.

Tip: Disc margin is INSIDE the peripapillary scleral ring of Elschn Appropriate lens magnification correction: Superfield 1.5x, 90D

Disc size

• Disc size is extremely variable, large discs have laeven though the area of the neuroretinal rim is

a large cup–disc ratio may not necessarily be patConversely, pathological rim loss can be missed iespecially if generalized.

• Disc size can also be measured by using the smadirect ophthalmoscope This spot size can be use



The most reliable way to detect glaucomatous optic nemay be with serial optic nerve head photographs.

Repeated scanning laser imaging is a promising approat l

The neuroretinal rim

The rim is more important than the cup. The cup defedge of the rim where most signs of glaucoma appe

The cardinal feature of glaucomatous optic neuropatissue from the inner edge of the rim.

Features that should raise suspicion that glaucomatoalready occurred include:12

• notching of the rim (especially to the disc margin)

• hemorrhage crossing the rim

• undercutting of the rim

• asymmetry of rim width between the eyes in the aasymmetry of disc size

• an abnormally thin rim in one or two sectors

An approximate rule is that a vertical cup–disc ratio rim to the disc margin anywhere outside the tempor suggests glaucoma. This rule may not apply if the dislarge or very tilted.

ISNT rule

Normally, the thickest to thinnest parts of the neuroreoptic disc are Inferior Superior Nasal Temporal (ISNT).from this may help to detect glaucomatous damage.

Optic disc photography and imaging




Table 1.7: Optic disc/NFL assessment

• Defines state of optic nerve function.

• Defines visual impairment.

Automated perimetry.

When glaucoma is suspected on examination.

It is very important to understand the correct proced

visual field testing. Users should read and be familiarmanual.

Qualitative Quantitative

Direct ophthalmoscopy Disc photogrdigitalization

Slit lamp indirect ophthalmoscopyStereo disc p

Disc photograph optic disc an

Simultaneous stereophotography Confocal laseophthalmosc

Nerve fiber layer photography(red-free fundus photography) Laser polarim

Optical CoheTomography

Why?

What?

When?

How?

Tips for better visual fields (see Appendix 4: How

Visual field examination



Characteristics of glaucomatous visual field defect

• Asymmetrical across horizontal midline.*

• Located in mid-periphery* (5–25 degrees from fixati

• Reproducible.

• Not attributable to other pathology.

• Clustered in neighboring test points (localized).

• Defect should correlate with the appearance of the neighborhood.

*early/moderate cases

References:

1. Drance SM. The visual field of low tension glaucoma and shoc

neuropathy. Arch Ophthalmol 1977;95:1359–1361.2. Drance SM. Some factors in the production of low tension gla

1972;56:229–242.

3. Drance SM, Sweeney VP, Morgan RW, et al . Studies of factors production of low tension glaucoma. Arch Ophthalmol 1973;8

4. Drance SM. Some studies of the relationships of haemodynamin open angle glaucoma, Trans Ophthalmol Soc UK 1968;88:63

5. Rochtchina E, Mitchell P, Wang JJ. Relationship between age the Blue Mountains Eye Study. Clin Experiment Ophthalmol 2

6. Foster PJ, Machin D, Wong TY , et al . Determinants of intraocassociation with glaucomatous optic neuropathy in Chinese STanjong Pagar Study. Invest Ophthalmol Vis Sci 2003;44:3885–

7 L JS L SH O m BS t l R l ti hi b t i t l

Other tests of optic nerve function

• Short wave length automated perimetry (blue on

• Frequency doubling perimetry




Treatmen



1.2 Treatment Categories and Targets

Tailor treatment to severity of glaucoma, depending onrisk factors.

Group 1: Glaucoma with high risk of progressive v

Definite glaucomatous optic neuropathy (GON) with co

field (VF) loss (moderate to advanced).

• Includes moderate to advanced normal pressure glau

Group 2: Glaucoma with moderate risk of visual losuspect with high risk of visual loss

• Mild GON with correlating early VF loss.

• Mild to moderate NPG.2

• Ocular hypertension ≥30 mmHg with suspicious disc.

• Primary angle closure with high intraocular pressureanterior synechiae (PAS).

• Angle neovascularization.

Group 3: Glaucoma suspect at moderate risk of vis• Glaucoma-like disc appearance without detectable V

• Fellow of eye with established GON (exclude secondglaucomas).4

• Ocular hypertension with suspicious disc.3

Group 4: Glaucoma suspect with low risk of visualMore important:

• ocular hypertension3,4

• older age3,4

l d bl l ( iti ll l d ith t PAS

Why?

Whatare the

categories?




Less important:

• steroid responder, steroid users• myopia, peripapillary atrophy (PPA)

• diabetes mellitus

• uveitis

• systemic hypertension.

Multiple risk factors (RFs)

The presence of multiple RFs proportionally increasesmay elevate a patient to Group 3.

Each visit.

Modifiable mechanisms for RFs.

To maintain functional vision throughout the patientminimal effect on quality of life.

Goal of intervention is risk factor reduction (RFR

• IOP.

• Angle control.

T f di i di /f (di b

Other risk factors

• Genetic risk factors:– family history– ethnicity

• Vascular risk factors:– hypertension– reduced perfusion pressure

– nocturnal hypotension

• Myopia

• Diabetes m

• Vasospasm– migraine– Raynaud’

• Sleep apne

When?

How?

Objective

Setting goals

Treatmen



Stage of disease

Use the four treatment categories above.

Estimate rate of neural lossHigher → more aggressive RFR.

Severity of RFsHigher or greater number → more aggressive RFR.

Modifiers of goals• Life expectancy.

• Ability to attend follow-up.

• Diseases that prevent accurate disc or field assessme

Goals of angle control• Deepen peripheral angle closure (AC).

• Iridotomy – reduce pupil block.

• Argon laser peripheral iridoplasty (ALPI) – flatten pe

• Lens extraction (LE) – reduces pupil block, displaces i

• Vitreous surgery.

IOP landmarks

Presenting (untreated) IOP.IOP in fellow normal eye in unilateral secondary glauco

Population mean and standard deviation IOP for norm

IOP control

Target IOP

• Target IOP is based on the pressure reduction requ




Goals (target IOPs) in Group 1

Target pressure reduction of at least 30%,

1,4,5

or closepressure (7–12 mmHg if achievable safely).4–7

Goals in Group 2Target pressure reduction of at least 20%.4–7

Goals in Group 3Monitor closely for change.Treat if risk(s) increase(s) with target pressure reduct

Group 4Monitor, no treatment.

Goals of treating predisposing diseasesPrevent onset of GON by proper management of dise

References:

1. The Collaborative Normal-Tension Glaucoma Intervention Steffectiveness of intraocular pressure reduction in the treatmglaucoma. Am J Ophthalmol 1998;126:498–505.

2. Tezel G, Siegmund KD, Trinkaus K, et al . Clinical factors assocglaucomatous optic disc damage in treated patients. Arch Op2001;119(6):813–818.

3. Gordon MO, Beiser JA, James MS, et al . The ocular hypertenthat predict the onset of primary open-angle glaucoma. Arc2002;120:714–720.

4. Leske MC, Heijl A, Hussein M, et al . Factors for glaucoma protreatment: the early manifest glaucoma trial Arch Ophthalm



Section 2




2.1 Initiation of Treatment

Glaucoma is a progressive optic neuropathy: if left untmay go blind.

Assess patients as a whole with the aim of preservationIntraocular pressure (IOP) is the only known causal risk one that can be manipulated effectively.2

Mechanisms that elevate IOP:

• primary unknown cause

• angle closure with or without glaucoma

• secondary glaucomas (see Appendix 5: Secondary glaof management ).

In the presence or the likelihood of developing visual dinterfere with quality of life during the patient’s lifetim

• Demonstrable functional and structural defect

Multiple mechanisms for angle closure (refer to Appclosure mechanisms)

Angle closure is caused by different sites of blockageoccur at multiple levels simultaneously and/or sequen

• Site one: pupil block – iris bombé appearance

• Site two: anteriorly rotated ciliary processes that pforward and/or thick peripheral iris – plateau iris c

• Site three: lens induced forward displacement of tconfiguration

• Site four: aqueous misdirection with accumulationvitreous pushing the entire lens–iris diaphragm fo

Why should treatment be initiated?

What should betreated?

When totreat?




Treat the mechanism(s)

IOP reduction:• medication(s)

• laser

• surgery.

Correct the abnormal anatomy:

• laser

• surgery.

(Once any angle closure component has been appropmanagement is similar to open angle glaucoma).

Collaborate with colleague(s) to treat systemic proble

References:

1. Sommer A, Tielsch JM, Katz J, et al . Relationship between inprimary open angle glaucoma among white and black AmerSurvey. Arch Ophthalmol 1991;109(8):1090–1095.

2. The AGIS Investigators. The advanced glaucoma interventionrelationship between control of intraocular pressure and visu Am J Ophthalmol 2000; 130(4):429–440.

How totreat?



2.2 Medical Treatment

• Effective for majority of patients.

• Generally acceptable therapeutic index.

• Mostly acceptable to patients.

• Widely available.

Choice depends on mechanism of glaucoma as well as oto Patient Assessment ). For angle closure, medical treatappropriate after peripheral iridotomy (PI).

Table 2.1: Efficacy, safety and dosing frequency of vari

Drug classDaily

Dosage Efficacy Loc

Adrenergicagonists

2x to 3x ++ to +++ ++

β-blockers 1x to 2x +++ +

Carbonicanhydraseinhibitors

Topical

Systemic

2x to 3x

2x to 4x

++

++++

++

0

Cholinergics 3x to 4x +++ +++

Hyperosmoticagents

Statdose(s)

+++++ 0

Prostaglandinsand other lipid

Why?

What?




Table 2.2: Mechanism of action of different drug clas

Mechanism of action Drug class

Reduction ofaqueous inflow

Adrenergic agonists•

•

β-blockers

N•

•

•

β

•

Carbonic anhydrase

inhibitors

S

•

•

•T

•

•

Increase in

Cholinergics

• Increase trabecularoutflow

•

•



n d i c a t i o n s *

C o m m o n d r u g

i n t e r a c t i o n s

L o c a l s i d e e f f e c t s

S

y s t e m i c s i d e e f f e

c t s

m i n e o x i d a s e

o r t h e r a p y

a n 2 y e a r s o

l d

C N S d e p r e s s a n

t s

( a l c o h o l , b a r b i t u r a t e s ,

o p i a t e s , s e d a t i v e s , o r

a n e s t h e t i c s ) , t r i c y c l i c

a n t i d e p r e s s a n

t s

B u r n i n g

, s t i n g i n g ,

b l u r r i n g ,

f o r e i g n - b o d y

s e n s a t i o n ,

i t c h i n g ,

h y p e r e m i a ,

f o l l i c u l a r

c o n j u n c t i v i t i s

O r a l d r y n e s s ,

h e a d a c h e ,

f a t i g u e ,

d r o w s i n e s s

t e l y

n d i c a t e d i n

i a l a s t h m a ,

o b s t r u c t i v e

n a r y d i s e a s e

,

a r d i a ,

h e a r t

u s e d

u s l y i n c a r d i a

c

S y s t e m i c β - b l o

c k e r s ,

c a l c i u m c

h a n n

e l

b l o c k e r s

B u r n i n g

, s t i n g i n g ,

p h o t o p

h o b i a ,

i t c h i n g ,

t e a r i n g

, d e c r e a s e d

c o r n e a l s e n s i t i v i t y ,

h y p e r e m i a , p u n c t a t e

e p i t h e l i a l k e r a t o p a t h y

B r o n c h o s p a s m ,

h y p o t e n s i o n ,

b r a d y c a r d i a ,

h e a r t

b l o c k , m a s k

h y p o g l y c e m i a ,

a d v e r s e l y a f f e c t s l i p i d

p r o f i l e ( e x c e p t

c a r t e o l o l ) , l o s s o f

l i b i d o ,

f a t i g u e ,

a g g r a v a t i o n o f

m y a s t h e n i a g r a v i s ,

d e p r e s s i o n , m e m o r y

i m p a i r m e n t , r e d u c e d

e x e r c i s e t o l e r a n c e ,

i n c r e a s e d f a l l s

i n t h e e l d e r l y

y

A s f o r n o n - s e l

e c t i v e

A s f o r n o n - s e l e c t i v e





C o m m o n d r u g



S


c t s

y d i c a t e d w i t h

m i s e d c o r n e a

l

i u m ,

i d e a l l e r g y

B u r n i n g

, s t i n g i n g ,

i t c h i n g , p u n c t a t e

e p i t h e l i a l k e r a t o p a t h y ,

b l e p h a r o c o n j u c t i v i t i s

B i t t e r t a s t e

m i d e a l l e r g y ,

n e s / f a i l u r e ,

r y / m e t a b o l i c

h y p o k a l e m i a

S t e r o i d s , d i u r e

t i c s ,

d i g o x i n

T r a n s i e n t m y o p i a

F a t i g u e ,

l e t h a r g y ,

a n o r e x i a ,

g a s t r o i n t e s t i n a l u p s e t ,

w e i g h t l o s s ,

p a r e s t h e s i a ,

t a s t e

d i s t u r b a n c e ,

S t e v e n s -

J o h n s o n S y n d r o m e ,

b l o o d d y s c r a s i a s , r e n a l

s t o n e s , h y p o k a l e m i a

e o v a s c u l a r

i n d u c e d

a s

P a i n , d

i m n e s s o f v i s i o n ,

b l u r r i n g

, m y o p i c s h i f t ,

r e t i n a l d

e t a c h m e n t ,

a g g r a v a

t e p u p i l l a r y

H e a d a c h e , s a l i v a t i o

n ,

l a c r i m a t i o n , u r i n a r y

f r e q u e n c y , d i a r r h e a

,

a b d o m i n a l c r a m p s




C o m m o n

d r u g



S


c t s

u r e ,

r y e d e m a ,

u r e

w i t h

s i o n

N A

H e a d a c h e s ,

u n p l e a s a n t t a s t e ,

h e a r t f a i l u r e ,

p u l m o n a r y e d e m a ,

d e a t h

y d i c a t e d i n

n c e o f a c t i v

e

a t o r y o c u l a r

n s , c y s t o i d

e d e m a

f o l l o w i n g

t e d

a r s u r g e r y

C h r o n i c p i l o c a

r p i n e

u s e m a y r e d u c e

e f f i c a c y o f t h e

s e

a g e n t s

B l u r r e d

v i s i o n ,

b u r n i n g , s t i n g i n g ,

c o n j u n c t i v a l

h y p e r e m i a ,

f o r e i g n

- b o d y

s e n s a t i o n ,

i t c h i n g ,

i n c r e a s e d

i r i s / p e r i o r b i t a l s k i n

p i g m e n

t a t i o n ,

l a s h

g r o w t h

, p u n c t a t e

e p i t h e l i a l k e r a t o p a t h y ,

c y s t o i d

m a c u l a r

e d e m a , r e a c t i v a t i o n

o f h e r p

e t i c i n f e c t i o n

A s f o

r i n d i v i d u a l c o m p o n e n t s




Choose the most appropriate medication

• Greatest chance of reaching target.• Best safety profiles.

• Minimally inconvenient.

• Affordable.

Start low and slow• Minimal concentration.

• Minimal frequency.

One-eyed therapeutic trial

• Start treatment in the worse eye.

• Check the IOP response after 2–4 weeks.

• Assess side effects.

• If acceptable and effective, make treatment bilate

If response inadequate to achieve target pressure: sw

• Switch to different class of medication (switching wagonist class may be useful, but compliance and reneed to be considered).

• Use the one-eyed therapeutic trial again.

Use more than one agent only if each has demonstrainsufficient to reach target

• Apply this principle also to the fixed combinations

How?



Teach the technique of drop instillation

• Demonstrate the preferred method including punctaeyelid closure for at least 3 minutes (‘double DOT’ –Technique, Don’t Open Technique).

• Ensure the patient can do it.

• If two or more drops being instilled, wait at least 5 mbetween drops.

• Provide educational material.

Suggested reading:

1. European Glaucoma Society. Treatment principles and optionGuidelines for Glaucoma, IInd edition, 2003, pp.3-1–3-45. Italy:

2. Ritch R, Shields MB, Krupin T. The Glaucomas – Glaucoma TheEd, Missouri: Mosby.

3. Hoyng PFJ, van Beek LM. Pharmacological Therapy for Glauco2000;59:411–434.

4. Goldberg I. Drugs for glaucoma. Australian Prescriber 2002;25

5. Soltau JB, Zimmerman TJ. Changing paradigms in the medicaglaucoma. Survey of Ophthalmology 2002;47(Suppl 1):S2–S5.

6. Kass MA, the Ocular Hypertension Treatment Study Group. Thtreatment study. A randomized trial determines that topical omedication delays or prevents the onset of primary open-angOphthalmol 2002;120:701–713.

7. Frishman WH, Kowalski M, Nagnur S, et al. Cardiovascular contopical, oral, and intravenous drugs for the treatment of glau

hypertension: focus on beta-adrenergic blockade. Heart Dis 2

8. Schuman JS. Antiglaucoma medications: a review of safety anrelated to their use. Clin Ther 2000 Feb;22(2):167–208.

9. Susanna R Jr, Medeiros FA. The pros and cons of different promanagement of glaucoma Curr Opin Ophthalmol 2001;12(2):




Figure 2.3: Medical Treatment Algorithm

Drug 1

Maximize compliance

Maxi

YES

Partial / side effeStop

Hold in reserve

Partial / side effe

Partial / side effeStop

Hold in reserve

Reaches target?Side effects none

/ tolerable?


/ tolerable?


/ tolerable?

Dr(if

Maxi



2.3 Laser Treatment

Laser treatment for open angle glaucoma

• Outflow enhancement: laser trabeculoplasty.

• Inflow reduction: cyclophotocoagulation (usually for

Laser treatment for angle closure (± glaucoma)• Pupillary block relief: laser iridotomy.

• Modification of iris contour: laser iridoplasty (goniop

• Inflow reduction: cyclophotocoagulation (usually for

• Relatively effective.• Relatively non-invasive.

Laser treatment to trabecular meshwork to increase ou

• Medical therapy failure or inappropriate.

• Adjunct to medical therapy.

• Primary treatment if appropriate.

Pre-laser management

• Explain the procedure.

• To reduce post-treatment intraocular pressure (IOP) inflammation, consider 1% apraclonidine1 or 0.2% b2–4% pilocarpine and/or β-blocker and/or steroid droprocedure.

• Topical anesthesia.

When?

Why?

What?

Laser trabeculoplasty

How?




Placement of laser spots

Between pigmented and non-pigmented trabecular m(see Appendix 7a: Argon laser trabeculoplasty ).

Parameters

Power: 300–1200 mw depending on the rSpot size: 50 µm (for Argon), 75 µm (for dioDuration: 0.1 sec (for Argon & diode), 3 ns f

Number of burns: 30–50 spots evenly spaced over 18remaining 180 degrees sequentially, or at the same t

Complications

• Temporary blurred vision.

• IOP spike with possible visual field loss.

• Transient iritis.

• Peripheral anterior synechiae if placement of burnpost-laser inflammation control is not effective.

• Endothelial burns of treatment too anterior.

• Chronic increase in IOP.

Post-laser management

• Continue any current medical treatment.

• Especially if IOP spike prevention treatment is not IOP at 1–6 hours after laser and again 24–48 hours

• Topical steroid qid for 4–14 days (consider omitting

Closer monitoring is suggested in certain cases

• Advanced glaucoma with severe field loss.

• One-eyed patient.

• High pre laser IOP

Iridotomy



• Effective.

• Relatively non-invasive.

• Preferable to surgical iridectomy.

Laser treatment to connect the anterior and posterior cpupillary block.

• Angle closure.

• Angle closure glaucoma.

• Occludable angle (absolute):

– angle closure in the fellow eye– confirmed family history of angle closure glaucoma

• Occludable angle (relative):

– need for repeated dilated examinations

– poor access to regular ophthalmic care.



• Instill 2% or 4% pilocarpine .

• To reduce post-treatment IOP spike/inflammation, co

1% apraclonidine1

or 0.2% brimonidine2

and/or β-blocarbonic anhydrase inhibitor and/or steroid drops be

• Topical anesthesia.

• Topical glycerin, if the cornea is edematous.

• Superior 1/3 of iris (beneath upper lids) desirable.

Laser:• Nd-YAG.

• Argon or krypton.

Why?

What?

When?

How?



Post-laser management

• Particularly if IOP spike prevention treatment is not IOP at 1–6 hours after laser and again at 24–48 hour

• Topical steroid at least 4–6 times/day for 4–14 days dinflammation.

• Verify the patency of the peripheral iridotomy (PI).

• Repeat gonioscopy.

• Pupillary dilatation to break posterior synechiae whe

• Reasonably effective.

• Relatively non-invasive.

• Adjunct to peripheral iridotomy.

Laser treatment to contract the peripheral iris:

• to flatten the peripheral iris

• to widen the anterior chamber angle inlet.

• Angle remains occludable following peripheral iridotom

• Help break an attack of acute angle closure.• Facilitate access to trabecular meshwork for laser tra

• Minimize the risk of corneal endothelial damage du



• Instill 2% or 4% pilocarpine.• To reduce post-treatment IOP spike/inflammation, co

1% apraclonidine1 or 0.2% brimonidine2 and/or β-blocarbonic anhydrase inhibitor and/or steroid drops be

• Topical anesthesia

Why?

Iridoplasty (gonioplasty)

When?

What?

How?




Endpoint

• Iris contraction with peripheral anterior chamber dvisible angle in line with the laser applications.

Complications

• Mild iritis.

• Corneal endothelial burns.

• IOP spikes.

• Peripheral anterior and/or posterior synechiae.

Post-operative treatment

• If IOP spike prevention treatment is not available, 1–6 hours and then 24–48 hours depending on the

• Topical corticosteroids 4–6 times/day for 7 days or the post-laser inflammation.

• Repeat gonioscopy to evaluate the anterior chambany other mechanism(s) of angle closure that mighintervention.

• Pupillary dilatation to break posterior synechiae w

Preferable to cyclocryoablation or cyclodiathermy.

Laser parameters

Power: 200 to 400 mW according to theSpot size: 200–500 µmDuration: 0.2–0.5 secNumber of burns: 30 to 50 applications over 360 d

least 1–2 spot diameters betwee

Why?

Cyclophoto-coagulation



Techniques

• Transpupillary.• Transscleral.

• Endolaser.

• Conservative, incremental applications avoiding 3 anpositions.

Non-contact transscleral Nd-YAG laser

Lasag Microruptor 2 using thermal mode.

Contact transscleral Nd-YAG laser

Continuous wave Nd-YAG laser with transscleral contac

Contact transscleral diode laser

Diode laser with transscleral contact probe (see Appentransscleral diode laser ).

Laser parameters

Power: 8–10 J and with maximum defocuposterior to the limbus

Number of burns: 32 over 360 degrees

Laser parameters

Power: 4–7 JDuration: 0.5–0.7 secNumber of burns: 30–40 over 360 degreesLocation: 1.0–2.0 mm from limbus

Laser parameters




Complications

• Pain.• Persistent inflammation.

• Loss of visual acuity.4,5

• Hypotony.6

• Scleral thinning.7,8

• Macular edema.

• Retinal detachment.9

• Aqueous misdirection syndrome.10

• Phthisis.11

• Sympathetic ophthalmia.12

• Failure to control IOP – multiple procedures may b

Post-operative management

• Analgesia.

• Continue any current treatment.

• Check IOP after 24–48 hours.

• Topical corticosteroids 4–6 times/day for 14 days orpost-laser inflammation.

• Cycloplegia 2–4 times/day for 7–14 days.

References:

1. Robin AL. Argon laser trabeculoplasty medical therapy to p

pressure rise associated with Argon laser trabeculoplasty. OJan;22(1):31–37.

2. Barnes SD, Campagna JA, Dirks MS, et al. Control of intraocafter Argon laser trabeculoplasty: comparison of brimonidi1.0%. Ophthalmol 1999 Oct;106(10):2033–2037.



8. Bhola RM, Prasad S, McCormick AG, et al . Pupillary distortion following trans-scleral contact diode laser cyclophotocoagulat

clinicopathological study of three patients. Eye 2001 Aug;15

(P9. Geyer O’Neudorfer M, Lazar M. Retinal detachment as a com

yttrium aluminum garnet laser cyclophotocoagulation. Ann OMay;25(5):170–172.

10. Hardten DR, Brown JD. Malignant glaucoma after Nd:YAG cyc Am J Ophthalmol 1991 Feb 15;111(2):245–247.

11. Trope GE, Ma S. Mid-term effects of neodymium:YAG transsclcyclophotocoagulation in glaucoma. Ophthalmol 1990;97(1):7

12. Lam S, Tessler HH, Lam BL, et al. High incidence of sympathetcontact and noncontact neodymium:YAG cyclotherapy. Ophth1992:99(12):1818–1822.




2 4 S



2.4 Surgery

Open angle glaucoma

• Outflow enhancement: penetrating and non-penetrsurgery.

• Glaucoma drainage device.

Chronic angle closure glaucoma

• Pupillary block relief: iridectomy.

• Outflow enhancement: trabeculectomy.

• Widening of anterior chamber angle inlet: lens extra

• Angle surgery: goniosynechialysis.


Acute angle closure (± glaucoma)

• Pupillary block relief: iridectomy.

• Outflow enhancement: trabeculectomy.

• Angle surgery: goniosynechialysis.

• Widening of anterior chamber angle inlet: lens extra

Childhood glaucoma

• Angle surgery: goniotomy and trabeculotomy.

• Outflow enhancement: trabeculectomy with or with


• Reasonably effective.1,2

• Reasonably safe.

• Widely available.

Why?



Use of anti-fibrotics insurgery



Scarring is the major cause for failure following filtratiAnti-fibrotics have been shown to inhibit scarring and success rate.

Commonly used: 5-Fluorouracil (FU), Mitomycin-C (MMOthers: β radiation.

• For high risk of failure following standard filtering s

repeat surgery, neovascular glaucoma, glaucoma in uaphakia, younger age, black race.

• In primary surgery, especially where a lower target prequired.11, 12

• To increase the success rates with artificial drainage

• With needling of a failed filter.

In these instances, the enhanced success rates with antthe complications associated with their use more accep

A. Application during surgery:

Dose

• Sponge soaked in MMC (varying doses of 0.2 to 0.4 m1–5 minutes), 0.4 mgs/mL for 1 minute for primary suconcentration for 3 minutes for poor prognosis filter

• Sponge soaked in 5-FU (50 mgs per mL) for 1–3 minu

• For subconjunctival use prior to needling of a bleb: aof MMC (0.4 mg/mL) and 0.02 mL of bupivicaine wit

Mode of application• Sponge placed under the conjunctiva. A little extra d

multiple sponges and a large surface area treatment

• If used prior to needling, 0.01 mL of MMC (0.4 mg/m

Why?

surgery

When?

What?

How?


over the area of injection may be tamponaded with



over the area of injection may be tamponaded with about 1 minute after the injection.

Note: The use of anti-fibrotic agents can be associated with sighcomplications and they must be used with caution. Use of an al

those experienced in the use of such agents is desirable.15

An implant allows aqueous to flow from the anteriomaintained episcleral space from where it can be abssurrounding blood vessels.

Molteno, Ahmed, Baerveldt.

Where there is a very high risk of failure of trabeculeanti-fibrotics – these eyes invariably have severe, refr

• Previously failed trabeculectomies with anti-fibrot

• Prior multiple ocular surgeries with conjunctival sc

• Traumatic, inflammatory or chemically induced sur

• Intraocular membrane formation likely to occlude

drainage procedure (e.g., irido-corneal endothelianeovascular glaucoma).

This surgery, and the management of the patient pocomplicated. An ophthalmologist with appropriate texperience should perform it.

Depending on the surgeon’s preference, one of the dpositioned on the scleral surface, usually in the supersuperonasal quadrant (or both for a two-plate implathe anterior chamber by an attached tube.

Why?

Glaucomadrainageimplants

When?

What?

How?




References:



References:

1. Nouri-Mahdavi K, Bigatti L, Weitzman M, et al . Outcomes o

primary open-angle glaucoma. Ophthalmol 1995;102:1760–

2. Jay JL, Murray SB. Early trabeculectomy versus conventionaopen angle glaucoma. Brit J Ophthalmol 1988;72:881–889.

3. European Glaucoma Society. Treatment principles and optioTerminology and Guidelines for Glaucoma, IInd edition, 2003

4. Ritch R, Shields MB, Krupin T. Glaucoma Surgery. In: The GlaTherapy ,1996, vol III, 2nd ed, pp.1633–1652. Missouri: Mosb

5. Broadway DC, Grierson A, O’Brien C, et al . Adverse effects omedication. II. The outcome of filtration surgery. Arch Opth1994;112(11):1146–1154.

6. Weinreb RN. Adjusting the dose of 5-fluorouracil after filtrside effects. Ophthalmol 1987;94(5):564–570.

7. Hurvitz LM. 5FU supplemented phacoemulsification, posterimplantation and trabeculectomy. Ophthalmic Surg 1993;24

8. Araujo SV, Spaeth GL, Roth SM, et al . A ten-year follow-up randomized trial of postoperative corticosteroids after trab1995;102(12):1753–1759.

9. Starita RJ, Fellman RL, Spath GL, et al . Short- and long-termcorticosteroids on trabeculolectomy. Ophthalmol 1985;92(7

10. Kolker AE, Kass MA, Rait JL. Trabeculectomy with releasablOphthalmol 1994;112(1):62–66.

11. Ramakrishnan R, Michon J, Robin AL, et al . Safety and effictrabeculectomy in southern India. A short-term pilot study.100(11):1619–1623.

12. Lamba PA, Pandey PK, Raina UK et al . Short-term results ofwith intraoperative or postoperative 5-FU for primary glauc1996;44:157–160.

13. Mardelli PG, Lederer CM Jr, Murray PL, et al . Slit-lamp needfiltering blebs using mitomycin C. Ophthalmology 1996;103

14. Khaw PT. Advances in glaucoma surgey: evolution of antimtherapy. J Glaucoma 2001;10(Suppl 1): S81–S84.

15. Khaw PT, Chang L, Wong TTL, et al . Modulation of wound surgey. Opin Ophthalmol 2001;12:143–148.



Section 3




3.1 Follow-up



p

The aim of follow-up is:

• to detect progression

• to detect effects of treatment

• to detect any change in health that may affect the gmanagement plan.

The follow-up process starts with the management plainitiation of therapy. At the follow-up visits the doctor

• briefly discuss the patient’s subjective well being and

• reassess risk factors: especially intraocular pressure (Igonioscopic change(s)

• reassess structure and function of the optic nerve• estimate rate of (any) progression

• identify adverse effect(s) of treatment

• assess compliance

• identify change(s) in current medical and ophthalmo

• discuss quality of life issue(s)

• reinforce appropriate patient information:– revise management– plan follow-up.

The more severe the damage, the worse the risk factorbe the follow-up.

• Patients will often wish to tell the doctor how they fhas (or has not) changed.

• This discussion helps build a good doctor–patient rel

Why?

What?

When?

Patient’s subjectivewellbeingand visual


Intraocular pressure (IOP)Reassess thei k f t



• IOP is the only currently modifiable risk factor for

• Assessment at every visit is vital.

• Establish whether target IOP has been achieved.

• A single measurement of IOP cannot detect all fluc

• Repeat unexpected readings at the same visit and

Gonioscopic changes

• Maintain baseline examination conditions.

• Perform gonioscopy regularly in patients with angperiodically in patients with open angles.

• Look for increased appositional and/or synechial c

• Pupil size changes have dynamic effects on the ang

• Look for change in angle width, synechiae, and pig

Causes of change in IOP at follow-up

Increased IOP:– progression of disease– gradual loss of efficacy of a drug (tachyphylaxi– poor compliance

• Reduced IOP:– therapeutic effect

• Reduced or increased IOP:– variation during the day and between days– change in systemic medications

risk factors

Optic discReassessstructure



Progression of GON usually occurs over a long period, wdetection of change difficult.

The occurrence of the following indicate GON progress Appendix 8: Glaucomatous optic neuropathy ):

• disc hemorrhage

• focal rim notching

• change in vessel position

• wedge-type nerve fiber layer defects

• generalized rim thinning

• increased cup–disc ratio.

Where baseline optic disc photographs and serial phot

available, detection of these changes is substantially enIf photographs are not available, the pupil should be dpossible to do this safely, consider prophylactic iridotomobtain an adequate view of the disc.1

Visual field

Change is frequent in perimetry. Usually only a small pto GON progression.

structure

and function of the optic nerve

Causes of change

• Learning – field performance usually improves oveattempts.

• Reliability changes, poor concentration may cause depression, look for false negatives.

• False negative errors may indicate progression. Falreflect poor reliability and may mask progression


Detecting progression



Progression is characterized by:• widening or deepening of an existing scotoma

• development of a new glaucomatous scotoma

• occasionally generalized field depression (althougby media opacity or miosis).

(Refer to Appendix 9: Field progression print-outs).

Changes in visual field should be confirmed by at learepeat tests.

There is a close correlation between glaucomatous chthe optic disc and consequent visual field loss.5, 6 Howconsiderable variation in morphology of a “normal” ability to perform visual field tests adequately.

Changes should be regarded skeptically until the devstandard deviation of serial measurements.

Adverse effects of treatment should be actively sougspecific questioning. These include:

• General effects: self-rated health, feelings about/atreatment.

• Systemic effects: respiratory, cardiovascular, digest

• Local effects: stinging/burning, blurring, itching, re

• The patient’s quality of life (QOL) should be estima

of the glaucoma management on QOL assessed.• This forms part of the assessment of burden of dis

treatment.

Quality of life issues

Identify adverseeffects of

treatment

SEAGIG DECISION SQUARE FOR GON



• The table below illustrates how various combinationprofiles and levels of disease stability/progression woaggressiveness of medical, surgical or laser intervent

• Intervention is graded +, ++, +++, with the last indicactive level of intervention.

• A +++ grade may be associated with a rapid, stepwisthrough medical to surgical management.

• A – indicates no addition to therapy.

Table 3.1: SEAGIG Decision Square for GON

Cop

Risk factors*

The following factors confer a higher risk of loss of visi

• high or rising IOP

• any appositional angle closure

• any peripheral anterior synechiae (PAS), or an increabefore

• longer life expectancy.*The more risk factors there are, the higher the risk. Thereforeadditional risk factor.

Risk Disease statu

Stable Uncertain

Increased + ++

Uncertain Reassess risk Reassess both

Stable – Reassess diseas


THE GLAUCOMA LIFE STORY (GLS)



The determinants of the GLS are:• state of damage

• life expectancy

• rate of progression.

The graph plots life expectancy against the extent ofdamage at diagnosis. The slope of the line is the rateis determined by risk factors Although rate is the key

Diagnosis

Damage

0

100

50

Increasing aggressiveness of trea

Medium riskfactors

Low

Highriskfactors

I n c r e a s i n g d a m

a g e

Normal aging attrition

Follow-up timing

Th t t i th IOP t hi h it i b li d th



The target pressure is the IOP at which it is believed th

vision for the rest of his/her life. However this needs totime to time.

Follow-up timing is determined by the treatment regimchanged. If the patient is stable the timing is determinextent of damage: for glaucoma suspect, 6–24 months;6–12 months; moderate damage, 4–6 months; severe d

References:

1. Kirwan JF, Gouws P, Linnell AET, et al . Pharmacological mydriaexamination. Br J Ophthalmol 2000;84:894–898.

2. Budenz DL, Feuer WJ, Anderson DR. The effect of simulated cglaucomatous visual field. Ophthalmology 1993;100:511–517.

3. Lam BL, Alward WL, Kolder HE. Effect of cataract on automatOphthalmology 1991;98:1066–1070.

4. Smith SD, Katz J, Quigley HA. Effect of cataract extraction onautomated perimetry in glaucoma. Arch Ophthalmol 1998;11

5. Quigley HA, Katz J, Derick RJ, et al . An evaluation of optic disexaminations in monitoring progression of early glaucoma da1992;99:19–28.

6. Yamagishi N, Antón A, Sample PA, et al . Mapping structural dto visual field defect in glaucoma. Am J Ophthalmol 1997;123




Case Detection



The Epidemiology section outlines our current understamagnitude of glaucoma blindness in Asia. This large buquestion of screening the population to detect and inittreatment for glaucoma.

The World Health Organization recommends that certa

be fulfilled before any population-based screening is u

• The disease must be an important public health prob

• There must be a recognizable latent or early stage, dpersons with the disease can be identified before sym

• There must be an appropriate, acceptable and reasoscreening test.

• There must be an accepted and effective treatment the disease that must be more effective at preventininitiated in the early asymptomatic stage than whensymptomatic stages of the disease.

• The cost of case finding must be economically balanpossible expenditure on medical care as a whole.

Other questions that need to be asked before embarkiprogram are listed below.2

1. Does early diagnosis lead to improved clinical outcomvisual function and quality of life?

2. Can the health system cope with the additional clini

resources required to confirm the diagnosis and provfor those who screen positive for a chronic disease su

3. Will the patients in whom early diagnosis is achievedb t d ti d t t t i

Why case detect or screen?


Population-based screening versus case detectioWhat is thebest



Population-based screening2 Cas

Patients are sought, there is animplied pledge that the process isgoing to make them better butthis may not be true.

Relies on detepatients who for other comus out; we treof our ability

guarantee of Obliged to establish a diagnosisand treatment using sophisticatedtechniques, which may not bewidely available for generalscreening. Without the requisiteequipment, trained personnel andinfrastructure, screening is not justified.

The patients who turn out to befalse positives carry the burden ofbeing labelled. The consequencesmay be severe.3

Based on dete‘at risk’ patienprevalence ofThus, most ofbelow – tonomophthalmosco

have a reasonpredictive val

Patients who actually have the

disease but have tested negativeare given a clean bill of health,which can be dangerous.

Many countries in the region maynot have the requisiteinfrastructure to follow-up andcategorize test positives or eventreat them appropriately.

The general pimportant rolopen angle glOphthalmoscodoubling peria physician’s o

Screening cannot be a one-time Most elderly p

strategy?

Primary open angle glaucoma (POAG)



* Clinic-based study with selected normals which may overestimat

Primary angle closure glaucoma (PACG)

According to population-based studies in Western counprevalence of POAG is five times that of PACG.11,12 Howglaucoma blindness in the world is caused by angle cloA i l 75% f bj i h PACG i A i h

Test Sensitivity Specificity C

Tonometry At cut off of >21mm: • Poor sen

• Half of tPOAG haat a sing

47.1%5 92.4%5

Automatedperimetry

97%6 84%6 • Test can specific o

• Time-con

Frequencydoublingperimetry

90–94%7–9* 91–96%7–9* • Rapid

• Relativel

Disc and nervefiber layerexamination

Cup–disc ratio of0.55 cut off:

• Best perflamp bio60, 78 or

• Direct opreasonab

• Inter-obs

disc exammethodsphotogra

59%10 73%10


Methods to identify eyes at risk of angle closure includepth as well as anterior chamber depth/axial length



and specificity of these techniques do not make themscreening.

Other easier techniques include the flash light test anIn the flash light test a light is shone from the tempocornea, parallel with but anterior to the iris. A shadoidentifies an eye with a shallow anterior chamber, atsensitivity of the flash light test is 80–86% and specif

The van Herick test uses a slit beam to compare the pchamber depth with the thickness of the cornea. Thespecificity of the test is 61.9% and 89.3%, respectivetest in decimals yields similar results.16

The flashlight and van Herick tests are also inapprop

their own.

If the van Herick test is positive AND the IOP is raisedimproves to 99.3%. This is high enough actually to trhaving angle closure.

Population-based screening

This is not recommended as a strategy. Population-baespecially inappropriate for developing countries witinfrastructure. Adequate infrastructure here implies texpertise (trained ophthalmologists), time and instruto confirm the diagnosis among test positives in an aIt also means the availability of expertise (trained sur

instrumentation to treat appropriately those in whomconfirmed. The operative word is “appropriate” and preferred practice. The requirements for diagnosis ancovered in the relevant sections.

Recommend -ations

Test Ideal AcceptableLess than

ideal



Tonometry Applanationtonometry

Tonopen Pneumo-tonometeror Schiötztonometer

Dilatedevaluation ofthe optic disc

Dilatedstereoscopicevaluation by

slit lamp bio-microscopy,fundusphotography

Directophthalmo-scope

Slit lampbiomicroscopyand van Hericktest

NA NA NA • The flaHerick tappropangle c

• A positHerick tconfirm

• If the flnegativiris on tpupil co

AND thnegativchambe1/4 thicperipheoccludaunlikelygonioscof rulin

angle m

Gonioscopy Indentationgonioscopyusing a Sussman

Goldmannsingle or twomirror with

• Mandaglaucom

f h


Currently, the optimal method for detection of indivis periodic routine comprehensive eye examinations.



depends on the current state of the healthcare systemcountry. In lieu of the ideal, case detection should be

Definitions

The predictive value of a test is dependent on the prin the population being tested. As shown in Figure 1factors remain constant, the positive predictive value

with increasing prevalence.

Figure 1: Positive predictive value (PPV)

Screening Population-based detection of g

Case detection(opportunisticscreening)

Active detection of glaucoma wclinics and hospitals for other pu

Prevalence The proportion of patients with(glaucoma) in the population te

Sensitivity The ability of a test to correctly

have glaucoma (true positives)

Specificity The ability of a test to correctly do not have glaucoma (true neg

Positivepredictive value

The proportion of patients withwho actually have glaucoma

Negativepredictive value

The proportion of patients withwho do not have glaucoma

With a low prevalence of glaucoma, most of those whofact be false positives.



In order to increase the effectiveness of all tests, the prglaucoma in the population to be tested must be reasoprevalence of glaucoma can be ‘increased’ by targetingsuch as the elderly, persons with family history of glauchypermetropes (angle closure) and myopes (open angl

References:

1. Wilson JMG, Jungner F. Principles and practice of screening foWHO, 1968, Public Health Papers No 34.

2. Sackett DL, Haynes RB, Guyatt GH, et al . Early diagnosis. In: C A basic science for clinical medicine, 1991, pp.153–170. Boston

3. Sackett DL, Haynes RB, Guyatt GH, et al . The Clinical ExaminaEpidemiology: A basic science for clinical medicine, 1991, pp.1Brown and Co.

4. Stamper RL. Glaucoma Screening. J Glaucoma 1998;7:149–150

5. Tielsch JM, Katz J, Singh K, et al . A population-based evaluatiscreening: the Baltimore Eye Survey. Am J Epidemiol 1991;134

6. Katz J, Sommer A, Gaasterland DE, et al . Comparison of analy

detecting glaucomatous visual field loss. Arch Ophthalmol 197. Quigley HA. Identification of glaucoma–related visual field ab

screening protocol of frequency doubling technology. Am J O1998;125:819–829.

8. Patel SC, Friedman DS, Varadkar P, et al . Algorithm for interpFrequency Doubling Perimeter. Am J Ophthalmol 2000;129:32

9. Thomas R, Bhat S, Muliyil JP, et al . Frequency doubling perime J Glaucoma 2002;11(1):46–50.

10. Quigley HA, Katz J, Derick RJ, et al . An evaluation of optic disexaminations in monitoring progression of early glaucoma da1992; 99:19–28.

11 Tielsch JM Sommer A Witt K et al Blindness and visual impa




Appendices

Appendix 1: How to test calibration oftonometer

1. Set the tonometer in position on its slit lamp stand, with its Pe



place and the tension on the circular dial on its right side (from

the slit lamp) set at 5 mmHg. The head should lean slightly for

examiner).

2. Slowly twirl the circular dial counter-

clockwise until the head rocks back towards

you. The tension should read 0–2 mmHg

below zero (Figure A).

3. Slowly twirl the dial clockwise until the head

rocks forwards again. The tension should

read 0–2 mmHg (Figure B).Figur

4. Remove the calibration rod from its box.

Firmly screw into position the holding

bracket that slides along the rod so that the

closest mark in front of the center one (i.e.,on the other side of the center from you) is

aligned as exactly as you can (Figure C).

5. Slip the rod and its holder into the

receptacle on the right side of the

tonometer. The head will rock backwards towards you.

6. Slowly twirl the circular dial clockwise until the head rocks for

reading on the dial: it should be 20–23 mmHg.

7. Slowly twirl the circular dial counter-clockwise until the head

tension on the dial should read 17–20 mmHg.

8. Remove the rod and holding bracket from

the tonometer and reposition the bracket so

that it is aligned exactly with the most

forward mark on the rod – furthest away

from you (Figure D).

9. Replace the rod in its bracket in the

tonometer receptacle. The tonometer head

Appendix 2: Tonometry mires



(Courtesy of Ivan Goldberg, Australia)

Excess corneal applanation (IOP lower than tonom

(Courtesy of Ivan Goldberg, Australia) (Courtesy of Ivan

Insufficient corneal applanation (IOP higher than to



Appendix 3b: Goniogram/gonioscopic

Grading system for gonioscopic findings (without inden

i k h d l hi k i



A. van Herick method uses corneal thickness as a unit

Grade 0 Iridocorneal contact

Grade I Peripheral anterior chamber depth betwendothelium is less than 1/4 corneal thick

Grade II Greater than 1/4 but less than 1/2 of cor

Grade III Greater than or equal to 1/2 of corneal t(non-occludable)

Grade 0 I II

1. Shaffer closed 10º 20º

2. Modified Schwalbe’s Schwalbe’s Anterior TMShaffer line is line is is visiblenot visible visible

B.

C. Spaeth

1. Iris insertion

Anterior to Schwalbe’s line or TMBehind Schwalbe’s line

Centered at scleral spur

Deep to scleral spur

Extremely deep/on ciliary band

2. Angular width

slit10º

20º

30º

Appendix 3c: Corneal wedge diagram



Appendix 4: How to optimize patient pin subjective perimetry

1 Choose the most appropriate investigation



1. Choose the most appropriate investigation• Test pattern – 24–2: early/moderate damage and gla

advanced damage or paracentral scotomas.

• Test strategy – e.g., SITA (Humphrey field analyzer): suspects.

2. Patient set-up at the perimeter

• Use near lens power based on current refraction.• Support the patient’s feet comfortably so that the th

• Support the patient’s back.

• Adjust chin rest height so the forehead touches its h

• Cover other eye fully – some patients prefer it open

• Support the arms so shoulders and neck do not tire.

3. Instructions to the patient before starting the test• “We are getting you to do this test to give us inform

how full and perfect your vision is, or if it isn’t, we wthe damage is, and what sort of damage it is.”

• “The test is not difficult, but to get the best informaneeds to be done in a particular way.”

• “The key to success is to look straight ahead all the

want them to look.) Let the light come to you – don• “You won’t see the light a good deal of the time, so

seems to be passing without a light appearing. The light very dim so that it can tell when you can just se

• “Press the button when you think you see the light.count – they can be fuzzy, dim, bright, it doesn’t ma

• “Blink whenever you need to, but do so when you pwill stop your eyes drying out and hurting, and you

• “Hold the button down when you want to rest. Thamachine. Release the button when you want to contcan rest as often as you like. You’re the one controll

• “Let’s have a practice run now so you can get a feel

Appendix 5: Secondary glaucomas – prmanagement

Strategy An example fo



Strategy An example fomanagement –

Diagnose the underlying cause(s) Diagnose uveit

Treat the underlying cause(s) Anti-infla

Identify the mechanism(s) Posterior synechi

Treat the mechanism(s) – Laser periphthey may change over the

course of the disease

Medical therapy first-line β-blockersagents are aqueous Carbonic anhy

inflow inhibitors

Appendix 6: Angle closure mechanisms

Site one: pupil block – iris bombé appearance



(Courtesy of Paul Chew, Singapore)

Site two: anteriorly rotated ciliary processes tha

forward and/or thick peripheral iris – plateau ir

Site three: lens induced forward displacement

volcano configuration

(Courtesy of Paul Chew, Singapore)

Appendix 7a: Argon laser trabeculopla



About 100 equally spaced laser spots (diameter 50 micr

seconds are applied over 360 degrees of trabecular me

t i f 180 d t d b 1 2 k Id

Copyright © 2003–2004 SEAGIG

Appendix 7b: Contact transscleral diod



Appendix 8: Glaucomatous optic neuro

Moderate g

optic neurop



p p• Localized lo

and superio

• A classic inf

arrows)

• Nerve fiber

superior andarea (large

Advanced gloptic neurop

• Neuroretina

• The cup exte

• Circumlinea

baring

• Bayoneting • Peripapillary

Nerve fiber l

(Courtesy of Prin RojanaPongpun, Thailand)

(Courtesy of Prin RojanaPongpun, Thailand)



Suggested Areas for Further Research

Prevalence and incidence of primary open angle glauco

angle closure glaucoma in Asia Pacific



Natural history of glaucoma in Asia Pacific

Natural history of angle closure

Risk factors – ranking risk factors among Asians accord

Normal values of central corneal thickness and optic diAsian countries

Applicability of ‘ISNT Rule’ in Asian eyes

Target pressure reduction – evidence on extent of redu

Clinical classification of angle closure glaucoma based u

outcomes

Clarification of mechanisms responsible for angle closu

Structural and functional change pattern, rate and extglaucoma versus open angle glaucoma

Randomized, controlled trials of all aspects of managem

closure – particularly roles of laser iridotomy, laser iridoextraction and filtering surgery

Treatment outcomes in angle closure glaucoma versus glaucoma – medical, laser and surgery

Efficacy of screening and prophylaxis of angle closure

Cost-efficient glaucoma screening program

Definition of Terms

Angle neovascularization New vessel formatio

surface of angle str

without formation

b



membrane.

Anterior ischemic optic Optic nerve head is

neuropathy (AION) from disturbance in

ciliary artery circula

Aqueous misdirection syndrome Misdirection of aqu

vitreous resulting fr

abnormality at the

zonule/anterior vitr

processes.

Cup–disc ratio (CDR) The fractional decim

dividing the cup dia

diameter. The closethe worse the dama

Glaucomatous optic Characteristic patte

neuropathy (GON) optic nerve head ca

Glaucoma suspect disc (GSD) Optic nerve head ap

suggestive of glauco

Neovascular glaucoma (NVG) Glaucoma resulting

fibrovascular memb

angle in response to

Normal pressure glaucoma (NPG) Characteristic glauc

neuropathy in the p

statistically normal

Occludable angle Clinical term for an

gonioscopically ope

enough to be consi

Pigment dispersion Abnormal scatterin

syndrome (PDS) into the anterior se

Plateau iris configuration An occludable anglepupil block.

Definition of Terms



p p

Plateau iris syndrome Angle closure in the

iridectomy.

Posner-Schlossman Syndrome Episodic anterior uv

trabeculitis with sec

of IOP.

Primary angle closure An eye in which app

suspect (PACS) between the periph

posterior trabecular

present or consider

Epidemiologically, t

defined as an angle

degrees of the post

meshwork cannot b

gonioscopically.

Primary angle closure (PAC) PACS with either sta

and/or peripheral a

Primary angle closure PAC with glaucomaglaucoma (PACG) neuropathy.

Primary open angle Chronic progressive

glaucoma (POAG) with characteristic c

nerve head and/or v

absence of seconda

Primary open angle Significant risk factoglaucoma suspect (e.g., ocular hyperte

history) and/or glau

in the absence of fr

Index

A

Adrenergic agonists, 33,34,35

factors influencing treatment,12

A l l

Gonioscopic changassessment at f

Gonioscopy, 17corneal wedge



Angle closureincidence, 5mechanisms, 31, Appendix 6signs of, 18surgery, 51

Anterior chamberdepth, risk factor for glaucoma, 6examination, 17

Anti-fibroticsuse in surgery, 53

B

β-blockers, 33,34,35factors influencing treatment, 13

C

Cataractcause of blindness, 5and glaucoma surgery, 55

Carbonic anhydrase inhibitorsfactors influencing treatment, 12

Cholinergics, 33,34,36

Cup–disc ratio, 20

Cyclophotocoagulation, 46

D

Disc haemorrhage, Appendix 8

treatment category, 25

Double DOT, 39

E

ggoniogram, Apmethods, Appetool for case de

H

Hyperosmotic agen

I

Intraocular pressurcauses of chanfactors influentargets, 27

Iridoplastylaser, 45modifiers of tr

Iridotomylaser, 43modifiers of tr

Iris examination, 17

ISNT rule, 21

L

Lensexamination, 1extraction, 27

N

Neuroretinal rim, 2

O

P

Perimetryautomated, 22frequency doubling, 23, 71

how to optimize patient performance,Appendix 4i i bl f

Surgery, 51penetrating filnon-penetratinuse of anti-fibr

Slit lampexamination, 1minimum acce

Index



minimum acceptable resources forexamination, 14

tool for case detection, 71

Peripapillary atrophy, 18treatment category, 25

Pigment dispersion syndrome

treatment category, 25

Posner-Schlossman syndromepast ophthalmic history of, 12

Primary open angle glaucomaepidemiology, 5, 69surgery, 51

Primary angle closure glaucoma

epidemiology, 7, 65surgery, 50

Prostagladins and other lipid receptoragonists, 33, 34, 37

Pseudoexfoliation syndrometreatment category, 25

RRetinal nerve fiber layer examination, 19

Risk factorsreassessment at follow-up, 60reduction, 26

S

Scotoma, 62, Appendix 9

SEAGIG decision square, 63

Secondary glaucomaf i l bli d 5

minimum acceexamination

tool for case de

Synechiaeperipheral anterisk factor for p

treatment cate

T

Tonometrytool for case deGoldmann-styl

tonometry, 1how to test cal

measurement eminimum acceexamination, 1Tonopen, 15Perkin’s tonom

Trabeculoplastylaser, 41, Appe

V

van Herick techniqtool for case de

Visual fieldcauses of chancharacteristics

defects, 23

examination, 2treatment cate



ISBN 0-9751692-0-3

apg guidelines nm view

Documents