Asia Pacific Glaucoma Guidelines

8/10/2019 Asia Pacific Glaucoma Guidelines

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


2/103

Copyright 20032004 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


3/103

A S I A P A C IGlaucoma Guide


4/103


5/103

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.


6/103

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)


7/103

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 DMellow (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


8/103

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


9/103

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


10/103

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


11/103

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


12/103

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 questionwhen?, 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


13/103

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.


14/103

Asia Pacific Glaucoma Guidelines


15/103

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 ofsymptomatic,acute angleclosure

Glaucomablindness


16/103


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. 82100,

2. Foster PJ, Johnson GJ. Glaucoma in China: how big is the p2001;85:12771282.

3. Teikari J, Raivio I, Nurminen M. Incidence of acute glaucom1982. Graefe's Arch Clin Exp Ophthalmol 1987;225:357360

4. Seah SKL, Foster PJ, Chew PT, et al. Incidence of acute primglaucoma in Singapore. An Island-Wide Survey.Arch Ophth1997;115:14361440.

5. Wong TY, Foster PJ, Seah SKL, et al. Rates of hospital admisclosure glaucoma among Chinese, Malays, and Indians in Si2000;84:990992.

6. Baasanhu J, Johnson GJ, Burendei G, et al. Prevalence and cvisual impairment in Mongolia: a survey of populations ageWorld Health Organization 1994;72:771776.

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

of Singapore. A cross-sectional population survey in TanjonOphthalmol2000;118:11051111.

8. Hong Kong Hospital Authority Statistical Report 20012002permanent 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


17/103

Epidemio

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

Melbourne Visual Impariment Project. Ophthalmology1998;115. Mitchell P, Smith W, Attebo W, et al. Prevalence of open-angl

The Blue Mountains Eye Study. Ophthalmology1996;103:1661

16. Shiose Y, Kitazawa Y, Tsukuhara S, et al. Epidemiology of glaunationwide glaucoma survey.Jpn J Ophthalmol1991;35:1331

17. Leske MC, Connell AM, Wu SY, et al. Risk factors for open angBarbados Eye Study.Arch Ophthalmol1995;113(7):91824.

18. McNaught AI, Allen JG, Healey DL, et al. Accuracy and implicafamily history of glaucoma: experience from the Glaucoma InTasmania.Arch Ophthalmol2000;118(7):900904.

19. Foster PJ, Machin D, Wong TY, et al. Determinants of intraocuassociation with glaucomatous optic neuropathy in Chinese STanjong Pagar Study. Invest Ophthalmol Vis Sci2003;44(9):388

20. Trnquist R. Shallow anterior chamber in acute angle-closurestudy.Acta Ophthalmol1953;31(Suppl. 39):174.

21. Okabe I, Taniguchi T, Yamamtoo T, et al.. Age-related changechamber width.J Glaucoma 1992;1:100107.

22. Foster PJ, Alsbirk PH, Baasanhu J, et al. Anterior chamber depVariation with age, sex and method of measurement.Am J O1997;124:5360.

23. Mitchell P, Hourihan F, Sandbach J, et al. The relationship betwmyopia. The Blue Mountains Eye Study. Ophthalmology1999;

24. Krishnadas R, Nirmalan PK, Ramakrishnan R, et al. Pseudoexfopopulation of southern India: the Aravind Comprehensive EyeOphthalmol2003;135:8307.


18/103


19/103

Section 1


20/103



21/103

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


22/103

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 -blockers

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


23/103

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:



24/103


Social history

Consider:

How regularly can the patient attend?

Can the patient afford and comply with treatment?

How will having glaucoma affect the patients 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 6090D 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


25/103

How toperform

Goldmanntonometry?

Intraocular pressure (IOP) is the only modifiable risk fac

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

Every visit.

Ensure tonometer is calibrated (seeAppendix 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 36 mmHg

Central corneal Thicker corneas are associated with

thickness IOP measurements, thinner corneas depressed IOP measurements: apply13 mmHg/40 deviation from 525

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

When?

How toperformGoldmanntonometry?

Why?

What?

Slit lampexamination

tonometry



26/103


Table 1.3: Measurement errors associated with GAT8

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


27/103

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.

(SeeAppendix 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 lookfor?

When?

Gonioscopy



28/103

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.(seeAppendix 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)


29/103

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 (6090D).

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 toperform discexamination?

Optic nerve

head andretinalnerve fiberlayer



30/103

Table 1.6: Normal vertical cupdisc ratios for vertical

Disc diameter Mean cupdisc ratio1.0 0.261.2 0.331.4 0.391.6 0.451.8 0.502.0 0.55

Disc recording

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

Draw notches, shelving, loss to rimclock hours.

Record whether nerve fiber layer is visible and assedefects.

Record vertical cupdisc ratio in the narrowest parrecording the rimdisc 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 ElschnAppropriate 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 cupdisc 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


31/103

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 cupdisc ratio rim to the disc margin anywhere outside the temporsuggests 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 discphotographyand imaging



32/103

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 fieldexamination


33/103

Characteristics of glaucomatous visual field defect

Asymmetrical across horizontal midline.*

Located in mid-periphery* (525 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 Ophthalmol1977;95:13591361.2. Drance SM. Some factors in the production of low tension gla

1972;56:229242.

3. Drance SM, Sweeney VP, Morgan RW, et al. Studies of factors production of low tension glaucoma.Arch Ophthalmol1973;8

4. Drance SM. Some studies of the relationships of haemodynamin open angle glaucoma, Trans Ophthalmol Soc UK1968;88:63

5. Rochtchina E, Mitchell P, Wang JJ. Relationship between age the Blue Mountains Eye Study. Clin Experiment Ophthalmol2

6. Foster PJ, Machin D, Wong TY , et al. Determinants of intraocassociation with glaucomatous optic neuropathy in Chinese STanjong Pagar Study. Invest Ophthalmol Vis Sci2003;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



34/103

Treatmen


35/103

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?



36/103

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


37/103

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



38/103

Goals (target IOPs) in Group 1

Target pressure reduction of at least 30%,

1,4,5

or closepressure (712 mmHg if achievable safely).47

Goals in Group 2Target pressure reduction of at least 20%.47

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 Ophthalmol1998;126:498505.

2. Tezel G, Siegmund KD, Trinkaus K, et al. Clinical factors assocglaucomatous optic disc damage in treated patients.Arch Op2001;119(6):813818.

3. Gordon MO, Beiser JA, James MS, et al. The ocular hypertenthat predict the onset of primary open-angle glaucoma.Arc2002;120:714720.

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


39/103

Section 2



40/103


41/103

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 (seeAppendix 5: Secondary glaof management).

In the presence or the likelihood of developing visual dinterfere with quality of life during the patients 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 bomb 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 lensiris diaphragm fo

Why shouldtreatmentbe initiated?

Whatshould betreated?

When totreat?



42/103

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 Ophthalmol1991;109(8):10901095.

2. The AGIS Investigators. The advanced glaucoma interventionrelationship between control of intraocular pressure and visuAm J Ophthalmol2000; 130(4):429440.

How totreat?


43/103

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 +++ ++

-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?



44/103

Table 2.2: Mechanism of action of different drug clas

Mechanism of action Drug class

Reduction ofaqueous inflow

Adrenergic agonists

-blockers

N

Carbonic anhydrase

inhibitors

S

T

Increase in

Cholinergics

Increase trabecularoutflow


45/103

ndications*

Commondrug

interactions

Localsideeffects

S

ystemicsideeffe

cts

mineoxidase

ortherapy

an2yearso

ld

CNSdepressan

ts

(alcohol,barbiturates,

opiates,sedatives,or

anesthetics),tricyclic

antidepressan

ts

Burning

,stinging,

blurring,

foreign-body

sensation,

itching,

hyperemia,

follicular

conjunctivitis

Oraldryness,

headache,

fatigue,

drowsiness

tely

ndicatedin

ialasthma,

obstructive

narydisease

,

ardia,

heart

used

uslyincardia

c

Systemic-blo

ckers,

calciumc

hann

el

blockers

Burning

,stinging,

photop

hobia,

itching,

tearing

,decreased

cornealsensitivity,

hyperemia,punctate

epithelialkeratopathy

Bronchospasm,

hypotension,

bradycardia,

heart

block,mask

hypoglycemia,

adverselyaffectslipid

profile(except

carteolol),

lossof

libido,

fatigue,

aggravationof

myastheniagravis,

depression,memory

impairment,reduced

exercisetolerance,

increasedfalls

intheelderly

y

Asfornon-sel

ective

Asfornon-selective


46/103


47/103

ndications*

Common

drug

interactions

Localsideeffects

S

ystemicsideeffe

cts

ure,

ryedema,

ure

with

sion

NA

Headaches,

unpleasanttaste,

heartfailure,

pulmonaryedema,

death

y dicatedin

nceofactiv

e

atoryocular

ns,cystoid

edema

following

ted

arsurgery

Chronicpiloca

rpine

usemayreduce

efficacyofthe

se

agents

Blurred

vision,

burning,stinging,

conjunctival

hyperemia,

foreign

-body

sensation,

itching,

increased

iris/periorbitalskin

pigmen

tation,

lash

growth

,punctate

epithelialkeratopathy,

cystoid

macular

edema,reactivation

ofherp

eticinfection

Asfo

rindividualcomponents



48/103

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 24 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?


49/103

Teach the technique of drop instillation

Demonstrate the preferred method including punctaeyelid closure for at least 3 minutes (double DOT Technique, Dont 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.3-13-45. Italy:

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

3. Hoyng PFJ, van Beek LM. Pharmacological Therapy for Glauco2000;59:411434.

4. Goldberg I. Drugs for glaucoma.Australian Prescriber2002;25

5. Soltau JB, Zimmerman TJ. Changing paradigms in the medicaglaucoma. Survey of Ophthalmology2002;47(Suppl 1):S2S5.

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-angOphthalmol2002;120:701713.

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 Ther2000 Feb;22(2):167208.

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



50/103

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


51/103

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% b24% pilocarpine and/or -blocker and/or steroid droprocedure.

Topical anesthesia.

When?

Why?

What?

Lasertrabeculoplasty

How?



52/103

Placement of laser spots

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

Parameters

Power: 3001200 mw depending on the rSpot size: 50 m (for Argon), 75 m (for dioDuration: 0.1 sec (for Argon & diode), 3 ns f

Number of burns: 3050 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 16 hours after laser and again 2448 hours

Topical steroid qid for 414 days (consider omitting

Closer monitoring is suggested in certain cases

Advanced glaucoma with severe field loss.

One-eyed patient.

High pre laser IOP

Iridotomy


53/103

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 -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?



54/103

Complications

Temporary blurring of vision.

Laser parameters for Argon laser

Preparatory stretch burns:

Spot size 200500 m

Exposure time 0.20.5 sec

Power 200600 mW

Penetration laser burns:

Diameter 50 m

Exposure time 0.02 sec

Power 8001000 mW

For pale blue or hazel iris:

First step, to obtain a gas bubble:

Diameter 50 m

Exposure time 0.5 secPower 1500 mW

Second step, penetration through the gas bubble:

Diameter 50 m

Exposure time 0.05 sec

Power 1000 mW

For thick dark brown iris: (chipping technique)Diameter 50 m

Exposure time 0.010.02 sec

Power 15002500 mW

Choose and modify parameters depending on indiv


55/103

Post-laser management

Particularly if IOP spike prevention treatment is not IOP at 16 hours after laser and again at 2448 hour

Topical steroid at least 46 times/day for 414 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 -blocarbonic anhydrase inhibitor and/or steroid drops be

Topical anesthesia

Why?

Iridoplasty(gonioplasty)

When?

What?

How?



56/103

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, 16 hours and then 2448 hours depending on the

Topical corticosteroids 46 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: 200500 mDuration: 0.20.5 secNumber of burns: 30 to 50 applications over 360 d

least 12 spot diameters betwee

Why?

Cyclophoto-coagulation


57/103

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 (seeAppentransscleral diode laser).

Laser parameters

Power: 810 J and with maximum defocuposterior to the limbus

Number of burns: 32 over 360 degrees

Laser parameters

Power: 47 JDuration: 0.50.7 secNumber of burns: 3040 over 360 degreesLocation: 1.02.0 mm from limbus

Laser parameters



58/103

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 2448 hours.

Topical corticosteroids 46 times/day for 14 days orpost-laser inflammation.

Cycloplegia 24 times/day for 714 days.

References:

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

pressure rise associated with Argon laser trabeculoplasty. OJan;22(1):3137.

2. Barnes SD, Campagna JA, Dirks MS, et al. Control of intraocafter Argon laser trabeculoplasty: comparison of brimonidi1.0%. Ophthalmol1999 Oct;106(10):20332037.


59/103

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 ONeudorfer M, Lazar M. Retinal detachment as a com

yttrium aluminum garnet laser cyclophotocoagulation.Ann OMay;25(5):170172.

10. Hardten DR, Brown JD. Malignant glaucoma after Nd:YAG cycAm J Ophthalmol1991 Feb 15;111(2):245247.

11. Trope GE, Ma S. Mid-term effects of neodymium:YAG transsclcyclophotocoagulation in glaucoma. Ophthalmol1990;97(1):7

12. Lam S, Tessler HH, Lam BL, et al. High incidence of sympathetcontact and noncontact neodymium:YAG cyclotherapy. Ophth1992:99(12):18181822.



60/103

2 4 S


61/103

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?


Childhood surgery


62/103

Childhood surgery

Goniotomy (primary treatment to be performed

Trabeculotomy (primary treatment to be performe

Failed medical and/or laser treatment.1

Anticipated failure of medical/laser treatments (e.g

Patient preference.

Other forms of therapy are inappropriate: compliaand/or socioeconomic problems.

Pre-operative assessment

Identify risk factors for failure and treat where applic

Asian, African, Hispanic ethnicity.

Previous surgery.

Young age.

Aphakia.

Pseudophakia.

Active ocular inflammation.

Prolonged use of topical glaucoma medications.5

Tendency to form keloids.

Neovascular glaucoma.

Surgical technique

Select appropriate technique.

When?

How?

Enhancement of surgery Use of anti-fibrotic agents:

intra-operative4

post-operative4,6,7

U f i i fl

Use of anti-fibrotics insurgery


63/103

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: 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 m15 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 13 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


64/103

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 surgeons 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?

Cataract and glaucoma are both common conditions aCataract and


65/103

Cataract and glaucoma are both common conditions aco-exist. A recent review has assessed current surgical m

Table 2.4: Evidence for surgical management of catara

Evidence grades:

A strongB moderateC weakI insufficient

For the surgical management of coexisting cataract andsome evidence of efficacy for using MMC.

*Extracapsular cataract extraction.

Cataract andglaucoma

surgery

Review comments

MMC (but not 5-FU) has a small benefit (24 mmHg) for ECCE*-trabeculectomy

Two-site surgery provides slightly lower IOP (13 mmthan one-site surgery

IOP is lowered more (13 mmHg) by phacoemulsificatthan by ECCE in combined procedures

Two-staged versus combined procedures

Alternative glaucoma procedures versus trabeculectoin combined procedures


References:


66/103

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 Ophthalmol1988;72:881889.

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.16331652. Missouri: Mosb

5. Broadway DC, Grierson A, OBrien C, et al. Adverse effects omedication. II. The outcome of filtration surgery.Arch Opth1994;112(11):11461154.

6. Weinreb RN. Adjusting the dose of 5-fluorouracil after filtrside effects. Ophthalmol1987;94(5):564570.

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):17531759.

9. Starita RJ, Fellman RL, Spath GL, et al. Short- and long-termcorticosteroids on trabeculolectomy. Ophthalmol1985;92(7

10. Kolker AE, Kass MA, Rait JL. Trabeculectomy with releasablOphthalmol1994;112(1):6266.

11. Ramakrishnan R, Michon J, Robin AL, et al. Safety and effictrabeculectomy in southern India. A short-term pilot study.100(11):16191623.

12. Lamba PA, Pandey PK, Raina UK et al. Short-term results ofwith intraoperative or postoperative 5-FU for primary glauc1996;44:157160.

13. Mardelli PG, Lederer CM Jr, Murray PL, et al. Slit-lamp needfiltering blebs using mitomycin C. Ophthalmology1996;103

14. Khaw PT. Advances in glaucoma surgey: evolution of antimtherapy.J Glaucoma 2001;10(Suppl 1): S81S84.

15. Khaw PT, Chang L, Wong TTL, et al. Modulation of wound surgey. Opin Ophthalmol2001;12:143148.


67/103

Section 3



68/103

3.1 Follow-up


69/103

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 patients 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 doctorpatient rel

Why?

What?

When?

Patientssubjectivewellbeingand visual


Intraocular pressure (IOP)Reassess thei k f t


70/103

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


71/103

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

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

disc hemorrhage

focal rim notching

change in vessel position

wedge-type nerve fiber layer defects

generalized rim thinning

increased cupdisc 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

andfunction ofthe opticnerve

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


72/103

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 toAppendix 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 patients 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 oflife issues

Identifyadverseeffects of

treatment

SEAGIG DECISION SQUAREFOR GON


73/103

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.

RiskDisease statu

Stable Uncertain

Increased + ++

Uncertain Reassess risk Reassess both

Stable Reassess diseas


THE GLAUCOMA LIFE STORY (GLS)


74/103

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

Increasingdam

age

Normal aging attrition

Follow-up timing

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


75/103

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, 624 months;612 months; moderate damage, 46 months; severe d

References:

1. Kirwan JF, Gouws P, Linnell AET, et al. Pharmacological mydriaexamination. Br J Ophthalmol2000;84:894898.

2. Budenz DL, Feuer WJ, Anderson DR. The effect of simulated cglaucomatous visual field. Ophthalmology1993;100:511517.

3. Lam BL, Alward WL, Kolder HE. Effect of cataract on automatOphthalmology1991;98:10661070.

4. Smith SD, Katz J, Quigley HA. Effect of cataract extraction onautomated perimetry in glaucoma.Arch Ophthalmol1998;11

5. Quigley HA, Katz J, Derick RJ, et al. An evaluation of optic disexaminations in monitoring progression of early glaucoma da1992;99:1928.

6. Yamagishi N, Antn A, Sample PA, et al. Mapping structural dto visual field defect in glaucoma.Am J Ophthalmol1997;123



76/103

Case Detection


77/103

The Epidemiologysection 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

Whycase detector screen?


Population-based screening versus case detectioWhat is thebest


78/103

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 notjustified.

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

Based on deteat 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 physicians o

Screening cannot be a one-time Most elderly p

strategy?

Primary open angle glaucoma (POAG)


79/103

* 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

9094%79* 9196%79* Rapid

Relativel

Disc and nervefiber layerexamination

Cupdisc 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


80/103

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 8086% 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


81/103

Tonometry Applanationtonometry

Tonopen Pneumo-tonometeror Schitztonometer

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.


82/103

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.


83/103

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: CA basic science for clinical medicine, 1991, pp.153170. 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;7:149150

5. Tielsch JM, Katz J, Singh K, et al. A population-based evaluatiscreening: the Baltimore Eye Survey.Am J Epidemiol1991;134

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

detecting glaucomatous visual field loss.Arch Ophthalmol197. Quigley HA. Identification of glaucomarelated visual field ab

screening protocol of frequency doubling technology.Am J O1998;125:819829.

8. Patel SC, Friedman DS, Varadkar P, et al. Algorithm for interpFrequency Doubling Perimeter.Am J Ophthalmol2000;129:32

9. Thomas R, Bhat S, Muliyil JP, et al. Frequency doubling perimeJ Glaucoma 2002;11(1):4650.

10. Quigley HA, Katz J, Derick RJ, et al. An evaluation of optic disexaminations in monitoring progression of early glaucoma da1992; 99:1928.

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



84/103


85/103

Appendices

Appendix 1: How to test calibration oftonometer

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


86/103

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 02 mmHg

below zero (Figure A).

3. Slowly twirl the dial clockwise until the head

rocks forwards again. The tension should

read 02 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 2023 mmHg.

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

tension on the dial should read 1720 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


87/103

(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 3a: Gonioscopy

Gonioscopy

Bi i i i ti f th t i h b


88/103

Biomicroscopic examination of the anterior chambe Essential for glaucoma diagnosis, treatment and pr

Methods

Gonioscopic contact lens permits the angle to be seen.

1. Direct gonioscopy

Place the Koeppe goniolens on an anesthetizedpatient supine. Fill the space between the lens a

a contact fluid (e.g., saline or methylcellulose). V

a handheld biomicroscope and an illuminator.

2. Indirect gonioscopy

At the slit lamp, place a mirrored lens (e.g., Gold

four-mirror indentation) on the cornea.

Indentation (pressure/dynamic) gonioscopy

With a four-mirror indirect contact lens press on the co

fluid into the angle to expose anatomic landmarks and

presence of peripheral anterior synechiae.

Appendix 3b: Goniogram/gonioscopic

Grading system for gonioscopic findings (without inden

i k h d l hi k i


89/103

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 10 20

2. Modified Schwalbes Schwalbes Anterior TMShaffer line is line is is visiblenot visible visible

B.

C. Spaeth

1. Iris insertion

Anterior to Schwalbes line or TMBehind Schwalbes line

Centered at scleral spur

Deep to scleral spur

Extremely deep/on ciliary band

2. Angular width

slit10

20

30

Appendix 3c: Corneal wedge diagram


90/103

Appendix 4: How to optimize patient pin subjective perimetry

1 Choose the most appropriate investigation


91/103

1. Choose the most appropriate investigation Test pattern 242: 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 patients feet comfortably so that the th

Support the patients 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 isnt, 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 wont 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 doesnt 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. Youre the one controll

Lets have a practice run now so you can get a feel

Appendix 5: Secondary glaucomas prmanagement

Strategy An example fo


92/103

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 -blockersagents are aqueous Carbonic anhy

inflow inhibitors

Appendix 6: Angle closure mechanisms

Site one: pupil block iris bomb appearance


93/103

(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


94/103

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 20032004 SEAGIG

Appendix 7b: Contact transscleral diod


95/103

Appendix 8: Glaucomatous optic neuro

Moderate g

optic neurop


96/103

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)


Appendix 9: Field progression print-ou

New scotoma


97/103

Deepening and enlarging scotoma


Suggested Areas for Further Research

Prevalence and incidence of primary open angle glauco

angle closure glaucoma in Asia Pacific


98/103

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


99/103

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.

Cupdisc 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


100/103

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


101/103

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


102/103

minimum acceptab

Date post:	02-Jun-2018
Category:	Documents
Upload:	drquan
View:	223 times
Download:	0 times

Asia Pacific Glaucoma Guidelines

Documents